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Background And Purpose: Previous studies have suggested embolic mechanisms for bihemispheric subcortical infarcts involving the anterior and posterior circulation. However, the mechanism of bihemispheric subcortical infarcts in middle cerebral artery (MCA) territories remains uncertain. We describe a patient with acute bihemispheric subcortical infarcts in restricted MCA territories suggesting an embolic mechanism.
Case Description: A 62-year-old woman with a history of hypertension and hyperlipidemia suddenly presented with left hemiplegia. Diffusion-weighted and T(2)-weighted magnetic resolution imaging of the brain showed multiple subcortical high intensity in the MCA territories. There were no acute infarctions in the cerebrum, brain stem, or cerebellum, including cortical lesions. The patient had no carotid, internal carotid artery, or MCA disease.
Conclusion: Bihemispheric subcortical infarcts in the MCA territory are likely to have a proximal embolic source and such infarcts could be associated with multiple subcortical infarcts due to small vessel disease.
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http://dx.doi.org/10.4137/CCRep.S7121 | DOI Listing |
Arch Physiol Biochem
September 2025
Department of GCP Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Background: Post-stroke cognitive impairment (PSCI), a common complication following stroke, significantly impacts patients' quality of life and prognosis. Research indicates that neuroregulation and protein metabolic disorders play crucial roles in the development of PSCI.
Purpose: This study aimed to evaluate the reliability of the Regional Meningoarterial Score (rLMC) in determining collateral circulation status in acute ischaemic stroke patients.
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.
Eur J Radiol
August 2025
Department of Radiology, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, China. Electronic address:
The mechanisms underlying the different morphological evolution of recent small subcortical infarcts (RSSIs)-ranging from cavitation to complete disappearance-remain incompletely understood. Free water (FW), derived from diffusion tensor image, has emerged as a sensitive marker reflecting various pathophysiological processes that may influence RSSI evolution. This study aimed to investigate whether baseline FW measures and their longitudinal changes are associated with the morphological evolution of RSSIs.
View Article and Find Full Text PDFMedicine (Baltimore)
August 2025
Department of Neurology, Shanghai Civil Aviation Hospital-Ruijin Hospital Gubei Branch, Shanghai, China.
Rationale: Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy is a rare genetic condition classified as a cerebral small vessel disease (CSVD). Traditionally, this disorder has been linked to either homozygous or compound heterozygous mutations in the high-temperature requirement A serine peptidase 1 (HTRA1) gene. Nevertheless, contemporary research has uncovered that heterozygous mutations in HTRA1 can also manifest in patients displaying patterns of autosomal dominant inheritance.
View Article and Find Full Text PDFNeurology
September 2025
Department of Clinical Genetics, Leiden University Medical Center, Leiden, the Netherlands.
Background And Objectives: Monoallelic cysteine-altering () variants cause the adult-onset small vessel disease cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), and biallelic loss-of-function () variants cause a rare, childhood-onset small vessel disease. Whether monoallelic variants also cause a small vessel disease is subject of debate. The aim of this study was to delineate the small vessel disease phenotype of individuals with a monoallelic variant and to compare it with CADASIL.
View Article and Find Full Text PDF