ArticleBrain communications2025
Post-stroke sensory hypersensitivity: insights from lesion-symptom and disconnection mapping.
Article in Brain communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Novel Compact Tactile Stimulator with Sensing: Designed for Individuals with a Brain Injury and MRI.IEEE transactions on medical robotics and bionics · 2026Article
- A neuropsychological perspective on sensory hypersensitivity after acquired brain injury.Brain communications · 2026Review
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Authors and funding
9 authors.
Funding
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Abstract
A post-injury increase in sensory sensitivity is frequently reported by acquired brain injury patients, including stroke patients. These symptoms are related to poor functional outcomes, but their underlying neural mechanisms remain unclear. Since stroke results in focal lesions that can easily be visualized on imaging, the lesions of stroke survivors can be used to study the neuroanatomy of post-injury sensory hypersensitivity. We used multivariate support vector regression lesion-symptom mapping and indirect structural disconnection mapping to uncover the lesion location and white matter tracts related to post-stroke sensory hypersensitivity. A total of 103 patients were included in the study, of which 47% reported post-stroke sensory hypersensitivity across different sensory modalities. The lesion-symptom and structural connectivity mapping identified the putamen, thalamus, amygdala and insula in the grey matter as well as fronto-insular tracts, and the fronto-striatal tract in the white matter as neural structures potentially involved in post-stroke sensory hypersensitivity. By examining the neuroanatomy of post-stroke sensory hypersensitivity in a large stroke sample, this study offers a significant advancement in our understanding of the neural basis of post-stroke sensory hypersensitivity.
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