Post-stroke spasticity (PSS), characterized by hyperreflexia and spastic hypertonia, is a common and debilitating consequence of cerebrovascular injury that impedes motor recovery. Despite its prevalence, the neurophysiological mechanisms underlying PSS remain poorly understood, partly due to the lack of reliable animal models. A known clinical correlate of spasticity is the weakened rate-dependent depression (RDD) of the Hoffman reflex (H-reflex), particularly in the upper limbs of chronic stroke patients. However, the mechanistic basis of RDD impairment and its relationship to brain lesion characteristics remain unclear. Here, we characterized the longitudinal progression of H-reflex RDD in a wrist flexor muscle following photothrombotic stroke in mice and examined its association with lesion volume across cortical and subcortical regions using magnetic resonance imaging. RDD was significantly reduced 2–3 weeks after stroke, indicating hyperreflexia. Approximately 60% of stroke mice exhibited weakened RDD. Notably, lesion volumes in contralateral primary (M1) and secondary (M2) motor cortices correlated positively with RDD impairment, linking greater cortical damage to more severe reflex hyperexcitability. These results suggest that damage to motor cortical regions disrupts central reflex-modulating pathways, contributing to post-stroke hyperreflexia. The presented stroke model provides a valuable platform for mechanistic investigations of PSS and for evaluating potential therapeutic interventions. • A longitudinal mouse model reproduces impaired H-reflex RDD after stroke. • RDD impairment emerges with delay and parallels clinical hyperreflexia. • Severity of RDD deficits correlates with contralateral motor cortex lesions. • Links cortical motor damage to spinal reflex hyperexcitability.
Kaul et al. (Sun,) studied this question.