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In acute ischemic stroke, reported relationships between lesion metrics and behavior have largely focused on lesion volume and location. However, hypoperfusion has been shown to correlate with deficits in the acute stage. Hypoperfusion is typically identified using perfusion imaging in clinical settings, which requires contrast. Unfortunately, contrast is contraindicated for some individuals. An alternative method has been proposed to identify hypoperfusion using hyperintense vessels on fluid-attenuated inversion recovery (FLAIR) imaging. This study aimed to validate the clinical importance of considering hypoperfusion when accounting for behavior in acute stroke and demonstrate the clinical utility of scoring the presence of hyperintense vessels to quantify it. One hundred and fifty-three participants with acute ischemic stroke completed a battery of commonly-used neurological and behavioral measures. Clinical MRIs were used to determine lesion volume and to score the presence of hyperintense vessels seen on FLAIR images to estimate severity of hypoperfusion in six different vascular regions. National Institutes of Health Stroke Scale (NIHSS) scores, naming accuracy (left hemisphere strokes), and language content produced during picture description were examined in relation to lesion volume, hypoperfusion, and demographic variables using correlational analyses and multivariable linear regression. Results showed that lesion volume and hypoperfusion, in addition to demographic variables, were independently associated with performance on NIHSS, naming, and content production. Specifically, hypoperfusion in the frontal lobe independently correlated with NIHSS scores, while hypoperfusion in parietal areas independently correlated with naming accuracy and content production. These results correspond to previous reports associating hypoperfusion with function, confirming that hypoperfusion is an important consideration-beyond lesion volume-when accounting for behavior in acute ischemic stroke. Quantifying hypoperfusion using FLAIR hyperintense vessels can be an essential clinical tool when other methods of identifying hypoperfusion are unavailable or time prohibitive.
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http://dx.doi.org/10.1016/j.nicl.2022.102991 | DOI Listing |
Neuroscientist
September 2025
Department of Neurology, School of Medicine, The Second Affiliated Hospital of Zhejiang University, Hangzhou, China.
Although intracerebral hemorrhage (ICH) and cerebral small vessel disease (cSVD) have long been considered distinct clinical entities, emerging evidence reveals significant overlap in their etiologies and imaging markers. This review aims to explore the relationship between ICH and cSVD, suggesting that ICH may represent an acute manifestation of small vessel disease. ICH is primarily caused by cerebral amyloid angiopathy and hypertension, while cSVD is mainly attributed to cerebral amyloid angiopathy and arteriolosclerosis.
View Article and Find Full Text PDFInt J Stroke
September 2025
Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Background: Endothelial inflammation is involved in cerebral small vessel disease (CSVD) pathogenesis. Vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) are biomarkers of endothelial inflammation.
Aims: This study investigated association of VCAM-1 and ICAM-1 with presence of CSVD and CSVD burden.
Neurol Genet
October 2025
Department of Neurology, National Taiwan University Hospital, Taipei.
Background And Objectives: Vascular NOTCH3 extracellular domain (NOTCH3ECD) deposition is the pathologic hallmark of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). We aimed to explore the relationships among the NOTCH3ECD deposition load, the variant genotype, and cerebral small vessel disease (SVD) severity.
Methods: Fifty-four individuals carrying pathogenic variants were enrolled and underwent skin biopsy for the quantification of dermal vascular NOTCH3ECD deposition load using immunohistochemical staining.
J Alzheimers Dis
September 2025
Department of Neurology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
BackgroundDisruptions of deep medullary veins (DMV) have been associated with the radiological severity and cognitive impairment observed in cerebral small vessel disease (SVD). Glymphatic dysfunction may serve as a potential mechanism underlying these associations.ObjectiveWe aimed to clarify the associations between DMV disruptions, MRI indices previously hypothesized as related to glymphatic function, white matter hyperintensities (WMH), and cognitive impairment in SVD.
View Article and Find Full Text PDFStroke Vasc Neurol
September 2025
Beijing Tiantan Hospital, Beijing, China
Rationale: Cerebral small vessel disease (CSVD) is responsible for 25% of ischaemic strokes and 45% of dementia cases. Currently, therapies targeting individual mechanisms have not shown significant efficacy. As CSVD involves multiple pathophysiological mechanisms, Cerebralcare pills, a traditional Chinese medicine with multiple pharmacological mechanisms, may be effective in treating cognitive dysfunction in CSVD.
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