ReviewPeerJ2026
Exploring new rehabilitation pathways for stroke based on the comorbidity of post-stroke hypoesthesia with anxiety and depression.
Review in PeerJ, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Central neuroendocrine dysregulation in ischaemic stroke sequelae: pathophysiological mechanisms-a narrative review.Frontiers in human neuroscience · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Post-stroke hypoesthesia is a common yet often overlooked sequela, involving diminished capacities in touch, temperature, and pain perception. Recent studies suggest that sensory deficits not only hinder functional recovery but also show a high rate of comorbidity with anxiety and depression. Objective: This study aims to systematically integrate the neural mechanisms, perceptual processing features, and behavioral consequences of post-stroke hypoesthesia and emotional disorders, to explore their comorbid relationship and propose more targeted rehabilitation strategies based on these mechanisms. Methods: This review conducts an interdisciplinary literature search, integrating research from neuroimaging, cognitive neuroscience, and rehabilitation medicine, including 73 relevant studies. The keywords used in the screening are "Hypesthesia," "Impaired Sensation," "Anxiety," and "Depression," covering studies on sensory impairments and mood disorders. By comparing the sensory-emotion interaction mechanisms in stroke and non-stroke populations, a bidirectional model is constructed. Results: Findings indicate that post-stroke hypoesthesia results not only from structural damage in regions such as the thalamus, insula, and prefrontal cortex, but also from functional disruptions in perceptual processing. These impairments contribute to a closed-loop mechanism involving neural dysconnectivity and predictive coding dysfunction, which facilitates the emergence of anxiety and depression. In turn, these emotional disorders further suppress sensory recovery, significantly reducing patients' motivation and rehabilitation compliance. Conclusion: Post-stroke hypoesthesia should be recognized as a critical etiological and maintaining factor in anxiety and depression. The coexistence of pathological and functional mechanisms underscores the need for rehabilitation strategies that transcend the boundaries of perception, emotion, and cognition. Developing a rehabilitation pathway centered on "sensory-emotional co-regulation" can facilitate early identification, subtype-specific intervention, and comprehensive support for emotional comorbidities following stroke.
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