The Achilles tendon (AT), which represents the conjoined tendon of the triceps surae muscles complex, is one of the largest, and strongest tendons of the human body [1]. However, as it serves as the primary plantarflexing mechanism of the ankle, the AT is also one of the most common sites of rupture. In the last years, the incidence of AT injuries has significantly increased within the middle-aged physically active population due to the growing popularity of some recreational sports [2]. Increasing evidence suggests that alterations in the muscle-tendon complex in response to altered loading and/or muscle contraction may not be restricted to the muscle alone but can also affect the fascial tissue. Ultrasonography (US) is currently considered a clinically reliable and non-invasive tool for delineating tendon, muscle, and fascial echotexture while detecting structural alterations, including thickening and echogenicity abnormalities [3]. In the present study, a comparative US imaging evaluation of textural features of the suro-Achilleo-plantar complex was performed both in healthy control and symptomatic subjects with mid-portion Achilles tendinopathy. Preliminary data demonstrate that, in symptomatic subjects, ultrasonographic alterations are not restricted to paratenon and intratendinous areas, but also affect upstream structures along the myofascial chain, resulting in thickening of the fascia interposed between medial gastrocnemius and soleus muscles. Moreover, positive correlations were found between soleus fascia thickening and abnormalities in AT, paratenon, and symptom severity. Interestingly, suro-Achilleo alterations comparable to those occurring in the symptomatic group were also found in a subgroup of asymptomatic subjects, suggesting that US myofascial alterations may be clinically significant in predicting a clinical outcome.

Can ultrasonographic evaluation of soleus fascial thickening be a useful predictor for Achilles tendinopathy?

Larisa Ryskalin
Primo
;
Gabriele Morucci
Secondo
;
Francesco Busoni;Paola Soldani
Penultimo
;
Marco Gesi
Ultimo
2023-01-01

Abstract

The Achilles tendon (AT), which represents the conjoined tendon of the triceps surae muscles complex, is one of the largest, and strongest tendons of the human body [1]. However, as it serves as the primary plantarflexing mechanism of the ankle, the AT is also one of the most common sites of rupture. In the last years, the incidence of AT injuries has significantly increased within the middle-aged physically active population due to the growing popularity of some recreational sports [2]. Increasing evidence suggests that alterations in the muscle-tendon complex in response to altered loading and/or muscle contraction may not be restricted to the muscle alone but can also affect the fascial tissue. Ultrasonography (US) is currently considered a clinically reliable and non-invasive tool for delineating tendon, muscle, and fascial echotexture while detecting structural alterations, including thickening and echogenicity abnormalities [3]. In the present study, a comparative US imaging evaluation of textural features of the suro-Achilleo-plantar complex was performed both in healthy control and symptomatic subjects with mid-portion Achilles tendinopathy. Preliminary data demonstrate that, in symptomatic subjects, ultrasonographic alterations are not restricted to paratenon and intratendinous areas, but also affect upstream structures along the myofascial chain, resulting in thickening of the fascia interposed between medial gastrocnemius and soleus muscles. Moreover, positive correlations were found between soleus fascia thickening and abnormalities in AT, paratenon, and symptom severity. Interestingly, suro-Achilleo alterations comparable to those occurring in the symptomatic group were also found in a subgroup of asymptomatic subjects, suggesting that US myofascial alterations may be clinically significant in predicting a clinical outcome.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11568/1240889
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