In the last decade, a large body of literature has characterized the brain as a complex network consisting of nodes and their connections, collectively termed the brain connectome. However, recent studies indicate added predictive value of connectivity-based measures, which capture perturbations of brain network connections or dynamics beyond focal lesion site (Ktena Sofia et al., 2019 Lopes et al., 2021b). Currently, common predictors of cognitive deficits and recovery include anatomical location, lesion severity, vascular risk factors, chronic brain pathology, and prestroke cognitive impairment (Bentley et al., 2014 Macciocchi et al., 1998 Munsch et al., 2016 Pendlebury, 2009). This heterogeneity in cognitive deficits after stroke arise not only from differences in the localization and extent of focal lesions, but also from potential secondary cascade effects in terms of altered brain connectivity (Rehme & Grefkes, 2013), and alterations of the hierarchical brain network structure (Stam, 2014). While some patients show considerable deficits and subsequent increased risk of neurodegeneration and dementia, others show no observable impairments. The magnitude and characteristics of cognitive impairments following stroke show substantial individual differences across patients. These findings demonstrate that the extent and distribution of structural disconnectivity following stroke are sensitive to cognitive deficits and may provide important clinical information predicting poststroke cognitive sequalae. Furthermore, our results indicated that disconnectivity within these clusters was associated with poorer performance across multiple cognitive domains. Multivariate analysis using Partial Least Squares on the disconnectome maps revealed that higher disconnectivity in right insular and frontal operculum, superior temporal gyrus and putamen was associated with poorer MoCA performance, indicating that lesions in regions connected with these brain regions are more likely to cause cognitive impairment. Cognitive performance was assessed in the whole sample using Montreal Cognitive Assessment, and a more comprehensive computerized test protocol was performed on a subset ( n = 82).
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To investigate the association between poststroke structural disconnectivity and cognitive performance, we estimated individual level whole-brain disconnectivity probability maps based on lesion maps from 102 stroke patients using normative data from healthy controls.
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One explanation building on recent work on brain networks proposes that the cognitive consequences of focal lesions are caused by damages to anatomically distributed brain networks supporting cognition rather than specific lesion locations. The location and size of focal lesions are only moderately predictive of the diverse cognitive outcome after stroke. Sequalae following stroke represents a significant challenge in current rehabilitation.