Background: Spasticity occurs after stroke and gives rise to substantial burden for patients and caregivers. Although it has been studied for many years, its definition continues to undergo reconsideration and revision. This partly reflects the diversity of its manifestations and that its pathophysiology, although well studied, is still debated.
Methods: A literature review was carried out to define the pathophysiology and risk factors for onset of post-stroke spasticity.
Results: It is clear that an acquired brain injury, including stroke, results in an imbalance of inhibitory and excitatory impulses that leads to upper motor neuron symptoms and that the location and extent of the lesions result in differing symptoms and degrees of spastic severity. The onset of spasticity is highly variable and may occur shortly or more than 1 year after stroke. The current understanding of spasticity onset is complicated by the role of contractures, which have been assumed to arise out of spasticity but may have a role in its cause. Other possibly predictive factors for the risk of post-stroke spasticity have been identified, including early arm and leg weakness, left-sided weakness, early reduction in activities of daily living, and a history of smoking.
Conclusions: Further understanding of spasticity risk factors is necessary for the development and integration of early interventions and preventive measures to reduce spasticity onset and severity.