ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2025
Sensory Deficits in Mice with Lateral Spinal Cord Hemisection Mimic the Brown-Séquard Syndrome.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 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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Who cites it
2 citing papers in PubMed.
- Spontaneous hemorrhage in the spinal canal leading to Brown-Séquard syndrome: a case report and review of the literature.Journal of medical case reports · 2026Review
- TAAR5 Modulates Sensorimotor Recovery After Spinal Cord Injury.Biomedicines · 2026Article
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15 authors.
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Abstract
Spinal cord injury (SCI) often results in permanent sensory deficits, significantly impairing the quality of life. These deficits are poorly addressed due to a lack of valid animal models with translational relevance. Here, we utilized a thoracic Level 8 lateral hemisection SCI mouse model (including both male and female mice) and applied a battery of behavioral assays requiring supraspinal transmission of sensory information. We also assessed ascending spinal circuits from the lumbar spinal cord to the brain. By 28 d post-SCI, sensory assessments revealed distinct deficits: reduced innocuous sensation in the ipsilateral hindpaw and enhanced sensation in the contralateral hindpaw. Both hindlimbs exhibited disrupted nocifensive behaviors, with chronic neuropathic dysesthesia observed only in the contralateral hindlimb. We provided anatomical evidence to elucidate the neural substrates responsible for these sensory discrepancies. This SCI mouse model mimics key features of human lateral hemisection conditions (Brown-Séquard syndrome) and offers a robust platform to explore underlying mechanisms and develop new therapeutic strategies.
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