Sensory Deficits in Mice with Lateral Spinal Cord Hemisection Mimic the Brown–Séquard Syndrome

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.