To examine whether sensory circuit injury drives motor impairments after pediatric stroke and to establish a preclinical model for developing circuit-specific neuromodulation therapies.

Pediatric stroke affects 1-2 per 1000 live births, causing lifelong motor impairments. Skilled movement requires both descending motor control and ascending sensory feedback. While bilateral motor compensatory projections from the uninjured hemisphere may support recovery, the sensory system lacks equivalent mechanisms. Our previous research study revealed that sensory pathway disruption more strongly predicts hand dysfunction than motor tract injury in children with hemiplegia. However, the independent contribution of sensory circuit damage to motor deficits cannot be isolated clinically. This project established a preclinical selective sensory lesion model to identify neuromodulation targets for movement recovery.

Electrolytic lesions demonstrated the highest specificity and reproducibility for targeting sensory tracts with mean lesion volume of 0.75±0.6 mm³. Viral tracing measured by integrated density confirmed significant sensory tract disruption in lesioned versus non-lesioned hemispheres (4.4±4.3×10⁶ vs 12.7±6.5×10⁶, p<0.01), while motor tract integrity was preserved (11.7±4.2×10⁶ vs 15.0±7.3×10⁶, p>0.05). Behavioral testing (N=8, 4M, 4F) showed sensory circuit lesions significantly impaired contralateral forelimb function (p<0.01), with motor deficits strongly correlating with sensory tract damage extent (r=0.61, p<0.05).

Selective sensory circuit disruption contributes to motor deficits after pediatric stroke, identifying sensory pathways as critical therapeutic targets. These findings provide a translational framework for precision rehabilitation utilizing neuromodulation to target sensory pathways to improve movement recovery after pediatric stroke.