Post-stroke spasticity (PSS), characterized by a velocity-dependent increase in muscle tone and exaggerated reflexes, affects a significant portion of stroke patients and presents a substantial obstacle to post-stroke rehabilitation. Effective management and treatment for PSS remains a significant clinical challenge in the interdisciplinary aspect depending on the understanding of its etiologies and pathophysiology. We systematically review the relevant literature and provide the main pathogenic hypotheses: alterations in the balance of excitatory and inhibitory inputs to the descending pathway or the spinal circuit, which are secondary to cortical and subcortical ischemic or hemorrhagic injury, lead to disinhibition of the stretch reflex and increased muscle tone. Prolongation of motoneuron responses to synaptic excitation by persistent inward currents and secondary changes in muscle contribute to hypertonia. The guidelines for PSS treatment advocate for a variety of therapeutic approaches, yet they are hindered by constraints such as dose-dependent adverse effects, high cost, and limited therapeutic efficacy. Taken together, we highlight key processes of PSS pathophysiology and summarize many interventions, including neuroprotective agents, gene therapy, targeted therapy, physiotherapy, NexTGen therapy and complementary and alternative medicine. We aim to confer additional clinical benefits to patients and lay the foundation for the development of new potential therapies against PSS.
Keywords: intervention; pathophysiology; spasticity; stroke.