Snapping phenomenon around the ankle: An anatomy-based review

Abstract

Ankle snapping occurs when tendons or retinacular structures abruptly move or slip over adjacent anatomical structures, often due to anatomical variations, pathological conditions, or acute injury. This phenomenon can cause pain and discomfort, ranging from mild irritation to debilitating symptoms that potentially disrupt daily activities and athletic pursuits. Considering the anatomy of the ankle, these snapping phenomena can be categorized into four regional groups: (1) Lateral; (2) Medial; (3) Anterior; and (4) Posterior. Lateral ankle snapping, a common occurrence, typically results from peroneal tendon subluxation due to compromise of the superior and inferior peroneal retinacula, or from intrasheath subluxation, characterized by abnormal tendon motion within an otherwise intact retromalleolar groove and retinaculum. Medial ankle snapping primarily affects the posterior tibial tendon and can involve the flexor digitorum longus tendon. Anterior ankle snapping results from abnormal gliding of the tibialis anterior tendon, extensor digitorum longus tendon, peroneus tertius tendon, and inferior extensor retinaculum. Posterior ankle snapping typically involves the plantaris tendon and flexor hallucis longus (hallux saltans). This mini-review comprehensively explores these snapping phenomena and their related pathologies in the foot and ankle, emphasizing the crucial roles of anatomical knowledge, thorough clinical assessment, and appropriate diagnostic and treatment approaches.

Key Words: Snapping ankle; Tendon subluxation; Tenosynovitis; Instability; Ankle pain

Core Tip: Snapping syndrome is characterized by the abrupt impingement or dislocation of anatomical or pathological structures that interact with adjacent tissues, manifesting as discomfort, pain, or functional limitation. Although this phenomenon has been documented in various joints, it remains relatively underrecognized in the ankle region. This mini-review presents an anatomically oriented approach, categorizing snapping phenomena into four directional groups–lateral, anterior, medial, and posterior. It highlights the importance of accurate clinical diagnosis, the role of imaging modalities, and guidance for appropriate treatment strategies.

INTRODUCTION

Snapping phenomena are characterized by an audible or palpable sharp and forceful sensation that occurs suddenly during movement. Clinically, these phenomena are significant not only for their audible or tactile manifestations but also for their association with a sense of instability (giving way), discomfort, debilitating pain, and functional impairment. Snapping syndromes have been reported across various anatomical regions, particularly adjacent to joints subjected to frequent movement[1-4]. These events typically result from the abrupt displacement of anatomical structures – most commonly tendons – over adjacent bony prominences or through fibro-osseous tunnels. The underlying pathophysiology of snapping phenomena is diverse, encompassing not only mechanical disturbances that compromise normal kinematics of anatomical structures, but also the contribution of non-anatomical pathologies, such as bony overgrowth, fracture fragments, hardware, or loose bodies.

The ankle possesses an intricate anatomical architecture, where densely packed tendons traverse confined tunnels stabilized by a complex retinacular system[5]. These retinacula are thickened regions of the superficial aponeurosis that serve as pulley-like structures, facilitating and stabilizing the tendon gliding. Injury, rupture, or inflammation of these tunnels or their retinacula, whether due to acute trauma or chronic repetitive loading commonly seen in sports activities, can lead to painful ankle pathologies. Among these, the terms ankle impingement and snapping ankle are often used, though they represent distinct clinical entities that can sometimes overlap. Ankle impingement refers to the entrapment or compression of soft tissues or bony structures within the ankle joint. It is characterized by pain during specific movements, often in the absence of a palpable or audible sensation. Conversely, snapping ankle is defined by a palpable or audible snapping or clunking sensation, resulting from the abnormal gliding of a tendon or other structure over a bony prominence. While some forms of snapping may cause pain, the defining characteristic is the mechanical sensation itself, which may not always be associated with significant discomfort. These two conditions can be distinct clinical entities; however, they are not mutually exclusive. For instance, a chronic snapping tendon may lead to inflammation and pain, eventually resulting in a subsequent impingement. Similarly, a space-occupying lesion that causes impingement may alter tendon mechanics, leading to a secondary snapping phenomenon. Due to this potential for overlap and inconsistent terminology in the literature, which leads to variability in clinical recognition and underreporting, the true prevalence of snapping ankle remains inadequately defined. This review aims to synthesize and highlight ankle snapping phenomena reported in the literature, categorized by anatomical structure (Table 1)[6-10].

Table 1 Summary of ankle snapping phenomena, categorized by anatomical region, includes the involved structures, pathologic findings, clinical presentation, relevant imaging findings, and both conservative and surgical management strategies.

Type		Involved structures	Pathologic findings	Clinical findings	Imaging findings	Conservative management	Surgical management
Lateral	Prefibular (anterior)	PL and PB	SPR tear; PL and PB dislocation	Snapping behind lateral malleolus during resisted eversion in dorsiflexed ankle	US: Tendon dislocation out of retromalleolar groove; MRI: Tendon tears, retinacular avulsions, tenosynovitis, and retromalleolar groove morphology	Immobilization with taping/plaster cast for 4-6 weeks (< 50% successful rate)	SPR repair/reconstruction ± groove deepening (open or endoscopic)
	Distal	PL	IPR tear; PL dislocation	Snapping tendon at peroneal tubercle with foot eversion	US: Tendon dislocation over peroneal tubercle; MRI: IPR tear		Peroneal tubercle resection, IPR reconstruction ± groove deepening (open or endoscopic)
	Intrasheath	PL and PB	Intact SPR; switching tendon positions	Snapping posterior to lateral maalleolus with ankle circumduction	US: Switching of tendon positions; MRI: Tendon split tear, intact SPR		Tendon debridement/repair ± SPR reconstruction and groove deepening (open or endoscopic)
Anterior		TA	Ganglion cyst at naviculocuneiform joint rubbing TA tendon	Snapping at tendon insertion during everted-to-inverted foot motion	Radiograph: Normal, US/MRI: No report	No report	Surgical excision
		EDL	IER incompetence; EDL snapping over lateral talar body	Snapping on anterolateral ankle during maximal foot inversion	MRI: No related pathology found	No report	IER repair/reinforcement
		PT	Hypertrophied PT muscle belly snapping over lateral talar dome	Snapping of fusioform mass anterolaterally with ankle plantarflexion-to-dorsiflexion	Radiograph: Normal, US/MRI: No report	No report	Arthroscopic myoplasty
		Talar head	Hypertrophied lateral talar head impinging on IER	Snapping anterolaterally in ankle dorsiflexion-plantarflexion, with foot inversion	Radiograph: Dorsolateral prominence of talar head; US: IER snaps over lateral prominence of talar head	No report	Arthroscopic taloplasty
Medial		PTT	Flexor retinaculum tear/pseudoretinaculum; PTT dislocation	Snapping/palpable cord-like structure over medial malleolus with resisted ankle plantarflexion-inversion	US: Tendon dislocation, retinacular tear or avulsion, fluid signal in retromalleolar region; MRI: Tendon dislocation, retinaculum lesions, associated deltoid ligament injury	Not specified (20% successful rate)	Flexor retinacular repair/reconstruction
		FDL	Retinacular detachment; Concurrent PTT and FDL dislocation	Snapping with resisted ankle plantarflexion and inversion	US/MRI: Tendon dislocation, retinacular detachment	No report	Flexor retinacular repair/reconstruction
Posterior		FHL	Stenosing FHL tenosynovitis	Triggering/Locking during great toe flexion, exaggerated in ankle plantarflexion	Radiograph: Os trigonum, Stieda's process, accessory ossicles, synovial chondromatosis; US: FHL tendon pathology/dynamic triggering; MRI: Tenosynovitis, stenosis, and fibrous bands	US-guided intralesional steroid injections (no success rate reported)	Pulley release/tenosynovectomy, excision of anomalous muscle belly
		Plantaris	Subluxable plantaris tendon to Achilles tendon	Snapping at posteromedial ankle or calf during squating maneuver	US: Subluxated plantaris tendon from medial to more posterior margin of Achilles tendon; MRI: Achilles tendon myotendinous junction edema without tendinopathy may be reported	Eccentric gastrocnemius stretching (no success rate reported)	Tendon resection/adhesion release

EDL: Extensor digitorum longus; FDL: Flexor digitorum longus; FHL: Flexor hallucis longus; IER: Inferior extensor retinaculum; IPR: Inferior peroneal retinaculum; MRI: Magnetic resonance imaging; PB: Peroneus brevis; PL: Peroneus longus; PT: Peroneus tertius; PTT: Posterior tibial tendon; SPR: Superior peroneal retinaculum; TA: Tibialis anterior; US: Ultrasound.

THE FOUR ANATOMICAL DIRECTIONS OF SNAPPING PHENOMENA IN THE ANKLE

Lateral ankle snapping

Snapping on the lateral aspect of the ankle reported in the literature is primarily caused by peroneal tendon instability (Figure 1). Anatomically, instability of peroneal tendon can occur at three distinct levels: (1) Prefibular or anterior type; (2) Peroneal tubercle or distal type; and (3) Intrasheath type.

Figure 1 Illustration of structures contributing to lateral ankle snapping: Peroneal tendons beneath the superior and inferior peroneal retinacula.

Prefibular (anterior) peroneal instability: At the level of the distal fibula, the peroneal longus and brevis tendons traverse a fibro-osseous retromalleolar groove beneath the superior peroneal retinaculum (SPR) (Figure 2). The SPR, originating approximately 2 cm proximal to the fibula tip and inserting via two bands into the Achilles tendon and the lateral aspect of the calcaneus, plays a pivotal role in maintaining tendon stability[11,12]. Histological analysis reveals its composition of dense collagen fibers with elastin, loosely affixed to the periosteum, rendering it susceptible to injury[13]. Disruption of the SPR can precipitate peroneal tendon subluxation or dislocation. The grading system, initially proposed by Eckert and Davis[13] and later modified by Oden[14], classifies SPR injuries into 4 types: (1) Grade 1 involves periosteal elevation of the SPR from the fibula; (2) Grade 2 describes an avulsion of the fibrocartilaginous rim from the fibula (also-called Bankart type); (3) Grade 3 signifies an avulsion of the cortical rim from the posterolateral fibula; and (4) Grade 4 denotes an avulsion or rupture of the posterior attachment, in which the tendon dissects through, with the SPR lying deep to the dislocating tendon (Figure 3).

Figure 2 Clinical images of anteriorly dislocated peroneal tendons (arrowhead) and the normal anatomical position of the peroneal tendons posterior to the lateral malleolus (arrow).

Figure 3 Illustration of the Eckert-Davis-Oden grading system for superior peroneal retinaculum injury.

Peroneal instability can result from either acute traumatic dislocation or nontraumatic events. Although traumatic peroneal tendon dislocation was historically misdiagnosed as a simple ankle sprain, recognition of the condition has increased since the 1980s[15]. Injury mechanisms typically involve forced dorsiflexion in conjunction with peroneal muscle contraction and torsional stress, particularly in activities such as skiing, skating, soccer, basketball, rugby, and ballet[11]. The provocative movement demonstrates snapping, with visible slipping of the tendons out of the groove behind the lateral malleolus during resisted eversion of the foot in a dorsiflexed ankle. Furthermore, a painful click may occur in cases of SPR attenuation accompanied by peroneus brevis (PB) subluxation and split tear, a finding known as a positive peroneal tendon compression test[16]. An anterior drawer sign should also be addressed as an indicator of anterolateral instability, which is a common concomitant injury due to the parallel orientation of the retinaculum to the calcaneofibular ligament. Nontraumatic causes of peroneal tendon instability include space-occupying lesions, such as retrofibular osteochondroma leading to peroneal tendon tear and subluxation[17], as well as hindfoot deformities. In pes planovalgus deformities, peroneal tendons can be pushed out by calcaneus valgus in a weight-bearing position[18].

Moreover, anatomical variants of the retromalleolar groove can predispose individuals to snapping phenomena. A low-lying PB muscle belly or a peroneus quartus (PQ) muscle may lead to abnormal movement of the peroneal tendons, especially in the presence of a flat or convex peroneal groove. A low-lying PB muscle belly has been reported to cause an overpacking phenomenon, resulting in SPR stretching and peroneal tendon subluxation[19]. Similarly, the PQ muscle – an accessory muscle present in approximately 20% of the population, typically originating from the lateral compartment or the lower third of PB muscle belly and inserting onto the peroneal tubercle on the calcaneus[20], can contribute to overcrowding and instability of the peroneal tendons[21].

Imaging modalities include plain radiographs, which might demonstrate any fracture as well as a fleck sign indicative of cortical avulsion (grade III injury). Magnetic resonance imaging (MRI) is considered the superior modality for assessing soft tissue integrity, evidence of tear or avulsion, or tenosynovitis for either the peroneal tendon, retinaculum, lateral ankle ligaments, and also retromalleolar groove morphology (Figure 4). Ultrasound (US) offers high sensitivity for peroneal tendinopathy and allows for dynamic visualization, despite its operator-dependent nature[22].

Figure 4 Magnetic resonance imaging shows dislocated peroneal tendons (arrow) and a torn superior peroneal retinaculum (dotted arrow), accompanied by a convex peroneal groove (arrowhead).

Management strategies for peroneal tendon instability vary based on the condition’s severity and chronicity, ranging from initial conservative measures to surgical intervention. Non-surgical treatment, including immobilization, non-steroidal anti-inflammatory drugs, and physical therapy, may be attempted, particularly for less severe or acute injuries, to facilitate healing of the retinaculum and periosteum[22]. However, the literature reports a high failure rate – approximately 50% in some studies – along with a higher incidence of pain and a lower return to baseline activity levels following conservative treatment. Consequently, surgical repair has become the mainstay of treatment in most cases[6,23]. Despites the generally low-likelihood of success with conservative treatment, recent systematic reviews suggest that a non-weight-bearing cast of at least 4-6 weeks may be a viable alternative, yielding successful outcomes in 60%-80% of cases[7]. When the surgery is needed, it is customized to the specific pathology and typically involves repair or reconstruction of the SPR and/or retromalleolar groove deepening. In contrast, other bone block procedures as well as rerouting procedures are reported less frequently in literatures, possibly due to their non-anatomical basis. Repair or reconstruction of the SPR is a cornerstone of treatment when the retinaculum is torn or avulsed (Figure 5), which could be done via open[24] or endoscopic approaches[25]. On the other hand, fibular groove deepening aims to create a more concave retromalleolar groove by fashioning an osteocartilagenous flap[25], thereby enhancing stability and preventing re-dislocation of the peroneal tendons (Figure 6). Although functional outcomes appear similar between isolated SPR repair and combined procedures with groove deepening[26,27], a higher return-to-sport rate has been reported in the latter group[6], reinforcing the notion that increased groove volume compromises peroneal tendon stability.

Figure 5 Post-repair intraoperative pictures of the superior peroneal retinaculum (arrowhead).

Figure 6 Intraoperative images of a groove deepening procedure: Creating an osteocartilagenous flap (arrow), impacting the underlying cancellous bone to deepen the groove before repositioning the peroneal tendons (dotted arrow). A postoperative computed tomography image demonstrates the recreated peroneal groove (arrowhead) and superior peroneal retinaculum repair using a suture anchor.

Furthermore, non-traumatic etiologies must be addressed. Low-lying muscle bellies and PQ muscles should be excised if identified, as should any other space-occupying lesions. One case report described peroneal tendon tearing and subluxation secondary to an osteochondroma arising from the retrofibular groove, which was successfully managed with excision of the osteocartilaginous mass, tubularization of the peroneus longus (PL) tendon, and groove deepening[17]. Additionally, correction of associated deformity is critical. For instance, in a case of bilateral pes planovalgus deformity with peroneal tendon dislocation, successful surgical management included medial displacement calcaneal osteotomy, groove deepening, and SPR repair[18].

Distal peroneal instability type: Providing stability for the distal peroneal tendons, the inferior peroneal retinaculum (IPR) originates from the inferior extensor retinaculum (IER) anteriorly and extends posteroinferiorly to insert onto the peroneal tubercle and the lateral calcaneal wall. At this level, the PL tendon typically passes inferior to the peroneal tubercle, while the PB tendon runs superiorly[28]. Although less commonly reported, an IPR tear can lead to PL dislocation at the peroneal tubercle level (Figure 7). The typical injury mechanism involves twisting ankle movements with the foot in a plantarflexed, abducted, and everted position, or a direct blow to the lateral aspect of the ankle. Clinically, patients present with pain during swift foot movements, and tendon dislocation can be reproduced with foot eversion. US is valuable for dynamically demonstrating PL tendon dislocation over the peroneal tubercle during foot eversion[29]. While MRI may show the dislocated tendon, it may not always reveal associated lesions, potentially limiting its contributory value in some cases[30]. Surgical treatment for this condition primarily involves removal of the peroneal tubercle, deepening of the peroneal groove on the lateral calcaneus, and IPR reconstruction[29,30].

Figure 7 Illustration of distal peroneal tendon instability. A: The inferior peroneal retinaculum stabilizes peroneal tendons at the level of the peroneal tubercle; B: Tear of the inferior peroneal retinaculum leads to dislocation of the peroneal longus tendon over the peroneal tubercle.

Intrasheath type: Intrasheath subluxation of the peroneal tendons, characterized by abnormal motion of the PB and PL relative to each other within the retromalleolar groove, was introduced by Raikin et al[31] to account for approximately 25% of patients with symptoms of peroneal tendon instability despite an intact SPR. This condition is further categorized into two types: (1) Type A, where the intact PB and PL tendons snap over each other, reversing their relative positions; and (2) Type B, where the PL tendon subluxates through a longitudinal split tear within the PB tendon (Figure 8)[31]. Again, US serves as a particularly effective diagnostic modality for intrasheath subluxation, capable of detecting transient anteroposterior tendon reversal that may not be evident on static imaging (Figure 9)[32]. Tendoscopy offers both diagnosis and therapeutic options for intrasheath peroneal subluxation while preserving the SPR[33,34]. Nonetheless, it is crucial to address associated pathology concurrently, including SPR reconstruction, debridement, tendon tear repair, and groove deepening procedures[33].

Figure 8 Illustration of the Raikin classification system for intrasheath peroneal subluxation.

Figure 9 Ultrasound images demonstrate the switching positions between the peroneus longus (arrowhead) and the peroneus brevis (arrow) tendons, occurring inside an intact superior peroneal retinaculum.

Anterior ankle snapping

Snapping on the anterior aspect of the ankle occurs beneath the superior extensor retinaculum (SER) and the IER. The SER is a rectangular fibrous band spanning from the lateral crest of the distal fibula to the anterior crest of the tibia above the tibiotalar joint[5]. The IER is a Y-shaped structure consisting of a medial root that inserts into the calcaneus anterior to the interosseous talocalcaneal ligament, and three lateral roots that extend into ligamentous structures within the sinus tarsi[35]. Within the compartment bordered by the anterior crests of the tibia and fibula lie four major tendons – the tibialis anterior (TA), extensor digitorum longus (EDL), extensor hallucis longus, and peroneus tertius (PT). All of which have been reported to cause anterior ankle snapping (Figure 10A).

Figure 10  Illustration of the structures contributing to ankle snapping. A: Illustration of the structures contributing to anterior ankle snapping - the tibialis anterior tendon, extensor digitorum longus tendon, peroneus tertius tendon, along with the talar head, all covered by the inferior extensor retinaculum; B: Illustration of anterolateral snapping due to an insufficient, torn, or scarred inferior extensor retinaculum, resulting in medial dislocation of the extensor digitorum longus tendon during foot adduction; C: Illustration of the structures contributing to medial ankle snapping - the tibialis posterior tendon and flexor digitorum longus traversing the tarsal tunnel, covered by the flexor retinaculum; D: Illustration of the structures contributing to posterior ankle snapping - the flexor hallucis longus and plantaris tendons.

TA tendon: Snapping of the TA tendon manifests as pain in the dorsomedial region near the tendon insertion, along with a snapping sensation aggravated by ankle motion. Goldman described a case with recurrent snapping during everted-to-inverted foot motion. This was attributed to a ganglion cyst extending from the naviculocuneiform joint. As conservative management failed to alleviate symptoms, the patient was successfully treated with surgical excision[36].

EDL tendon: The EDL tendons can also contribute to snapping due to destabilization of the IER, as reported by Cho et al[37]. They described a case of painful snapping at the anterolateral aspect of the ankle during maximal foot inversion, following an ankle twisting injury. The snapping could be prevented by applying pressure with the examiner’s index finger on the anterolateral corner of the talar body. Surgical exploration revealed loosening of the injured superficial layer of IER and medially snapping of EDL over the anterolateral corner of the talus as the navicular was adducted during foot inversion (Figure 10B). The patient was treated by lateralizing the superficial layer of the IER to limit navicular adduction over the talus, thereby preventing EDL displacement.

PT tendon: The PT muscle originates from the distal third of the anterior fibula, passes beneath the IER, and inserts on the dorsal surface of the fifth metatarsal. A case report describes a patient who exhibited anterolateral snapping and a concomitant fusiform mass. The snapping was reproducible with ankle dorsiflexion and internal rotation of the foot. Following failed conservative treatment, arthroscopy revealed a hypertrophied PT snapping over the lateral talar dome. Arthroscopic myoplasty, involving partial resection of the PT muscle belly, was effective in resolving the snapping phenomenon and allowed the patient to return to sport[38].

Talar head: Anterolateral snapping can also be caused by a hypertrophied talar head, where the IER becomes tensioned in an inverted foot position and impinges upon the uncovered lateral prominence of the talar head. This mechanism results in snapping during ankle dorsiflexion-plantarflexion with the foot inverted, which could be confirmed by US. Arthroscopic taloplasty performed to contour the talar head serves as the definitive treatment for this condition[39].

Medial ankle snapping

Snapping on the medial side of the ankle is caused by the posterior tibial tendon (PTT) and the toe flexor tendons, which traverse the tarsal tunnel within the retromalleolar fibro-osseous groove (Figure 10C). The flexor retinaculum, a fan-shaped fibrous band, extends from the medial malleolus to the posterosuperior aspect of the calcaneus and encloses the tarsal tunnel in continuity with the dorsal fascia of the foot and plantar aponeurosis, providing coverage and attachment to the tendon sheaths of the PTT, flexor digitorum (FDL), and flexor hallucis longus (FHL) tendons[40].

PTT: PTT dislocation can manifest as snapping. However, only approximately one-third of patients with PTT dislocation report this recurrent snapping sensation[8]. While the etiology of PTT dislocation can be non-traumatic[41] or iatrogenic, such as following tarsal tunnel release[42,43], most commonly occurring as a result of trauma. Delayed diagnosis of traumatic PTT dislocation is not uncommon, as it can be initially mistaken for ankle sprains, deltoid ligament injuries, PTT dysfunction, or tarsal tunnel syndrome. The typical injury mechanisms involve forceful dorsiflexion, including during squat loading[44], combined with inversion or eversion twisting forces. These mechanisms are commonly observed during falls[39,45] and in various sport activities such as karate, taekwondo, gymnastics, soccer, and snowboarding[46-50]. A shallow PTT groove has been suggested as a predisposing anatomical factor[51]. Clinical examination may reveal a subluxable PTT, palpable as a cord-like structure over the medial malleolus during resisted ankle plantarflexion-inversion[8]. Mahieu et al[52] proposed two types of PTT dislocation: (1) Type I, or subcutaneous dislocation, which results from rupture of the flexor retinaculum, leading to anterior displacement of the PTT over the medial malleolus; and (2) Type II, or subperiosteal dislocation, which arises from a periosteal avulsion of the flexor retinaculum at its tibial insertion site (Figure 11). Furthermore, Mullens et al[48] reported a case of PTT dislocation in which both midsubstance tear of the retinaculum and medial malleolus periosteal avulsion were present. MRI and US can demonstrate a dislocated tendon, along with a redundant (Figure 12), torn, or avulsed flexor retinaculum, often accompanied by fluid signal in retromalleolar region.

Figure 11  Illustration of the Mahieu classification system for posterior tibial tendon dislocation. PTT: Posterior tibial tendon.

Figure 12 Magnetic resonance imaging of the dislocated posterior tibial tendon (arrow) underneath the redundant flexor retinaculum (arrowhead).

The management of PTT dislocation is primarily surgical, as nonoperative treatment is often unsuccessful when the dislocated tendon lies within a pseudoretinaculum[53]. The goals of surgical management are to reduce the dislocated tendon, restore the mechanical support of the flexor retinaculum (Figure 13), and re-establish the retromalleolar groove[45]. The flexor retinaculum reconstruction procedures vary based on the retinacular pathology, whether it involves acute tears or chronic laxity. Direct repair with suture anchors[49,54] is a primary approach, particularly when the retinaculum is acutely torn. For cases involving chronic laxity or retinacular-periosteal sleeve formation, reconstruction techniques may involve passing sutures through the tibia[8,46], creating a cortico-periosteal flap from the medial malleolus[55], or employing a buttress plate anterior to the retromalleolar groove to reinforce the flexor retinaculum[48].

Figure 13 Intraoperative pictures of a pseudoretinaculum with a dislocatable posterior tibial tendon (arrow), and the reduced tendon beneath the repaired flexor retinaculum (arrowhead).

Crucially, associated pathologies that coexist with or result from PTT dislocation must also be addressed. PTT tear, intra-articular meniscoid-like scar tissue, impinged lateral osteochondral lesion of the talus, tarsal tunnel syndrome, and deltoid ligament injuries, all of which should also be appropriately treated[8,56].

FDL longus tendon: While less prevalent, FDL dislocation occurring concurrently with PTT dislocation following twisting injuries has been documented. Aguiar et al[57] reported a case of chronic medial malleolus pain after a motorcycle accident, where MRI and US revealed anterior dislocation of both tendons with retinacular detachment. Similarly, Padegimas et al[54] described concomitant PTT and FDL dislocation after an inversion injury sustained during basketball. In such cases, surgical intervention, involving tendon reduction and reattachment of the medial retinaculum, was necessary to address the pathology.

Posterior ankle snapping

Posterior ankle snapping, characterized by palpable or audible events extending from the calf to the plantar foot, is primarily attributed to the FHL and plantaris tendons (Figure 10D).

FHL: The FHL tendon originates from the lower two-thirds of the posterior aspect of the fibula, traversing the space between the posterior tubercles of the talus, coursing beneath the sustentaculum tali, and ultimately inserting onto the base of the distal phalanx of the hallux. Its trajectory is anatomically divided into three zones: (1) The segment from the myotendinous junction to the entrance of fibro-osseous tunnel; (2) The segment extending from the retrotalar tunnel to the knot of Henry; and (3) The final segment from the knot of Henry to its phalangeal insertion via the intersesamoid ligament[58]. Hallux saltans, also referred to as triggering big toe, represents a stenosing tenosynovitis or an entrapment of a hypertrophied FHL tendon confined within a constricted fibro-osseous tunnel[59]. The defining clinical feature is a sudden triggering or locking of the great toe during flexion, followed by an abrupt release during extension[9]. Triggering occurs more rapidly when the ankle is in plantarflexion[59,60]. Patients commonly report pain around the posteromedial part of the leg and ankle, or even the midfoot region, accompanied by a palpable or audible click at the retromalleolar area, which is typically exacerbated by great toe extension with the ankle in dorsiflexion. The etiology can be congenital, particularly in bilateral presentations[61], or acquired through chronic repetitive activities such as extreme and frequent plantarflexion in ballet dancers[62]. Radiographic evaluation of the ankle may reveal osseous abnormalities capable of impinging upon the FHL tendon, including the presence of an os trigonum, Stieda's process, accessory ossicles, or synovial chondromatosis[63]. US is a valuable imaging modality for delineating FHL tendon pathology and for dynamically visualizing fibrous bands that may restrict tendon excursion[60,63].

Initial management of FHL-related snapping and tenosynovitis typically involves conservative strategies. US-guided intralesional steroid injections have been reported as an effective intervention for reducing tendon sheath inflammation and alleviating symptoms[59]. In refractory cases, particularly those with chronic scar tissue formation from repetitive injury, surgical intervention may be necessary. This includes the release of the retinaculum and tenosynovial sheath of the FHL tendon via a posteromedial approach[61,62] or through endoscopic techniques (Figure 14)[60], resulting in immediate symptom relief. Additionally, anomalous extension of FHL muscle belly[62] and accessory FDL muscles[64] should also be identified and excised if present[59].

Figure 14 Arthroscopic view showing the release of the flexor hallucis longus tendon pulley (arrow), which exposes the flexor hallucis longus tendon underneath (arrowhead).

Plantaris tendon: The plantaris tendon, an accessory ankle plantarflexor that travels deep to the lateral head of gastrocnemius and is adjacent to the triceps surae before inserting medially onto the calcaneal tuberosity or the Achilles tendon[10], can also contribute to posterior ankle snapping. Snapping of the plantaris tendon is often characterized by a sudden pop during a twisting injury or as pain accompanied by a reproducible click along the posteromedial ankle, even without a reported injury[65]. Palpable snapping can be reproduced with maneuvers like squatting with knee flexion and ankle dorsiflexion, or resisted ankle plantarflexion[10,66]. US demonstrated a subluxable plantaris tendon from the medial to the more posterior margin of the Achilles tendon. While surgical tenotomy is a frequent treatment for symptomatic cases to enable return to activity[66], Miadlikowski et al[65] reported an instance where intraoperative adhesions between the plantaris and Achilles tendons were the primary finding. In their report, separation of these adhesions alone resolved the snapping, negating the need for tendon resection.

CONCLUSION

This mini-review provides a comprehensive exploration of the ankle snapping phenomenon, categorized by anatomical regions. Lateral ankle snapping most frequently results from peroneal tendon instability due to injury of the peroneal retinacular, often predisposed by anatomical variations. Anterior ankle snapping is associated with disruption or laxity of the extensor retinaculum, leading to subluxation of the TA, EDL, or PT tendons. Medial ankle snapping primarily involves dislocation of PTT, occasionally accompanied by FDL tendon involvement. Finally, posterior ankle snapping occurs along the course of FHL tendon and can also involve the plantaris tendon at the posteromedial of the heel. Clinical presentations range from not only acute traumatic events to misdiagnosed chronic conditions, but also other non-traumatic etiologies. Accurate diagnosis through careful physical examination, MRI, or US is essential for early recognition. Conservative treatment often yields poor results, likely because it cannot resolve or heal the significant abnormal gliding, subluxation, dislocation, or impingement of the affected structures. Surgical intervention is frequently required, aiming to restore normal retinacular and osseous groove anatomy to stabilize the involved tendons. Concurrently addressing any associated pathologies, whether they are causal or consequential, is crucial for achieving successful outcomes. Due to the paucity of literature, current conservative management algorithms remain limited in value. Developing detailed, structured treatment guidelines, supported by long-term follow-up and patient-reported outcome measures, will be essential to optimize both non-surgical and surgical management outcomes.