The anatomy and mechanisms of syndesmotic ankle sprains

To present a comprehensive review of the anatomy, biomechanics, and mechanisms of tibiofibular syndesmosis ankle sprains. MEDLINE (1966-1998) and CINAHL (1982-1998) searches using the key words syndesmosis, tibiofibular, ankle injuries, and ankle injuries-etiology. Stability of the distal tibiofibul...

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Veröffentlicht in:Journal of athletic training 2001-01, Vol.36 (1), p.68-73
Hauptverfasser: Norkus, S A, Floyd, R T
Format: Artikel
Sprache:eng
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Zusammenfassung:To present a comprehensive review of the anatomy, biomechanics, and mechanisms of tibiofibular syndesmosis ankle sprains. MEDLINE (1966-1998) and CINAHL (1982-1998) searches using the key words syndesmosis, tibiofibular, ankle injuries, and ankle injuries-etiology. Stability of the distal tibiofibular syndesmosis is necessary for proper functioning of the ankle and lower extremity. Much of the ankle's stability is provided by the mortise formed around the talus by the tibia and fibula. The anterior and posterior inferior tibiofibular ligaments, the interosseous ligament, and the interosseous membrane act to statically stabilize the joint. During dorsiflexion, the wider portion anteriorly more completely fills the mortise, and contact between the articular surfaces is maximal. The distal structures of the lower leg primarily prevent lateral displacement of the fibula and talus and maintain a stable mortise. A variety of mechanisms individually or combined can cause syndesmosis injury. The most common mechanisms, individually and particularly in combination, are external rotation and hyperdorsiflexion. Both cause a widening of the mortise, resulting in disruption of the syndesmosis and talar instability. CONCLUSIONS AND RECOMMENDATION: Syndesmosis ankle injuries are less common than lateral ankle injuries, are difficult to evaluate, have a long recovery period, and may disrupt normal joint functioning. To effectively evaluate and treat this injury, clinicians should have a full understanding of the involved structures, functional anatomy, and etiologic factors.
ISSN:1062-6050
1938-162X