Abstract
Equinovarus foot is one of the most commonly spasticity related conditions in stroke survivors, leading to an impaired gait and poor functional performances. Notably, spastic muscles undergo a dynamic evolution following typical pathophysiological patterns. Botulinum Neurotoxin Type A (BoNT-A) is the gold standard for focal spasticity treatment, and ultrasound (US) imaging is widely recommended to guide injections and monitor muscle evolution. The role of BoNT-A in influencing muscle fibroadipose degeneration is still unclear. In this study, we analyzed medial gastrocnemius (MG) and soleus (SOL) US characteristics (cross-sectional area, muscle thickness, pennation angle, and mean echo intensity) in 53 patients. MG and SOL alterations, compared to the unaffected side, depend on the spasticity only and not on the BoNT-A treatment. In functionally preserved patients (functional ambulation classification, FAC > 3; modified Ashworth scale, MAS ≤ 2), the ultrasonographic changes of MG compared to ipsilateral SOL observed in the paretic limb alone seems to be due to histological, anatomical, pathophysiological, and biomechanical differences between the two muscles. In subjects with poor walking capability and more severe spasticity, such ipsilateral difference was found in both calves. In conclusion, BoNT-A does not seem to influence muscle degeneration. Similar muscles undergo different evolution depending on the grade of walking deficit and spasticity.
Highlights
The first definition of spasticity was given by Lance in 1980 as a motor disorder characterized by a velocity-dependent increase in muscle tone with exaggerated tendon jerks, due to hyperexcitability of the stretch reflex, as a typical aspect of the upper motoneuron lesion [1]. 4.0/).Gracies and colleagues described the pathophysiology of spastic paresis, focusing on the motor control axis and its post-stroke evolution
Our findings strongly suggest that even a prolonged treatment with Botulinum Neurotoxin Type A (BoNT-A), characterized by several injection sessions per year, early followed by a cycle of intensive conventional neuromotor rehabilitation, does not influence muscle degeneration in a meaningful way
Our findings confirm that BoNT-A is a safe treatment for spastic equinovarus foot (SEF), that repeated injection cycles do not seem to induce fibroadipose infiltration in medial gastrocnemius (MG) and SOL, and that muscle degeneration appears to be primarily related to the spastic muscle evolution
Summary
Gracies and colleagues described the pathophysiology of spastic paresis, focusing on the motor control axis and its post-stroke evolution. The deficit of central nervous control causes a motor unit loss, leading to paresis, spasticity, overactivity, and, disuse and immobilization complications. This generates a vicious circle in which spasticity and disuse feed off each other [2]. Spastic muscle is a dynamic structure with complex evolution patterns that are still not completely clear. In stroke survivors affected by spastic paresis, a common clinical find is spastic equinovarus foot (SEF) due to an increased tone of plantar-flexor muscles (PF). TS is in charge of 80% of torque in plantiflexion [3] and is among the most commonly affected muscles in case of spasticity [4]
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