Postoperative Anti-NMDA Receptor Encephalitis Following Resection of an Insular Astrocytoma: A Case Report.

Extensive studies show that vascular dementia (VaD) is the second most common cause of dementia, accounting for up to 30% of cases, and cerebrovascular pathology contributes to cognitive decline in a substantial proportion of individuals with dementia of all kinds. Given global population aging and the modifiable nature of vascular risk factors, early identification of VaD at preclinical or earlier stage in the community settings has become a critical public health priority. Since the introduction of National Institute of Neurological Disorders and Stroke and Association Internationale pour la Recherche et l’Enseignement en Neurosciences (NINDS-AIREN) criteria in 1993, multiple professional societies have sought to standardize the diagnosis of vascular cognitive disorders. These works broadened the concept of VaD into a spectrum of vascular cognitive impairment. However, persistent challenges remain, including inconsistent terminology, variability in requirements of cognitive domains assessment, limited harmonization of subjective and objective criteria, and insufficient incorporation of advances in neuroimaging and biomarkers of cerebral small vessel disease (CSVD). These limitations have hindered comparability across studies and the translation of research findings into clinical applications, particular the community-based prevention strategies. To address these gaps, the International Society for Vascular Behavioural and Cognitive Disorders (VasCog Society), in collaboration with the World Stroke Organization, recently proposed revised criteria for vascular cognitive impairment and dementia (VCID) (VasCog-2–WSO criteria). The revised framework introduces several important advances. First, it establishes unified terminology across the VCID spectrum, explicitly defining preclinical VCID, vascular mild cognitive impairment (vaMCI), and VaD. Second, the revised VCID framework maintains the core VasCog-1 criteria, requiring both “objective” evidence of cognitive impairment and “subjective” cognitive or functional concerns to meet the criteria of vaMCI and VaD, strengthening diagnostic rigor. Third, rather than privileging specific cognitive domains, the criteria acknowledge that vascular brain injury may produce heterogeneous, multidomain patterns of impairment. Finally, the VasCog-2–WSO criteria integrate contemporary and standardized neuroimaging markers, particularly comprehensive MRI assessment of CSVD, to substantiate the vascular etiology. Despite these advances, timely evaluation of the VasCog-2–WSO criteria in preclinical, community-based populations remains limited. It remains uncertain whether the revised criteria effectively identify individuals at early stages of VCID and discriminates gradients in vascular burden and long-term clinical outcomes. We therefore sought to validate the VasCog-2–WSO criteria in a community-dwelling, dementia-free and stroke-free cohort by examining their screening yield, phenotypic differentiation across the defined VCID spectrum, associations with cardiovascular risk burden, and prognostic relevance for all-cause mortality.