In 1950, Wolin and colleagues⁹ were the first to describe a cause for anterolateral impingement. The study consisted of 9 patients with chronic pain and swelling to the anterolateral aspect of the ankle after an inversion ankle sprain. Upon surgical examination, patients were found to have a soft-tissue mass consisting of hyalinized tissue that the investigators identified as meniscoid lesions because of its resemblance to a torn knee meniscus. These fibrous adhesions are well-developed bands of scar tissue that occur from the anterior talofibular ligament and extend into the ankle joint, resting in the lateral gutter (Fig. 1). Upon removal of the meniscoid lesions, Wolin noted improvement of the patient’s symptoms. Initially thought to be torn ends of a ligament, histopathologic analysis revealed no ligamentous tissue.⁸ Several investigators have noted and attributed meniscoid lesions to the cause of anterolateral ankle pain.^10,11

Fig. 1 Meniscoid lesion. (A) Sagittal T2 MRI demonstrating anterior joint effusion with a loose body (arrow) noted on the anterior lip of the tibia. Joint effusion with increased signal intensity is noted around os trigonum. (B) Arthroscopic image reveals meniscoid lesion. (C) After partial resection with probe demonstrating no associated articular damage.

Synovitis may also occur after an inversion ankle sprain.⁸ The sprain may damage the anterior talofibular ligament (ATFL), anterior inferior tibiofibular ligament (AITFL), or the calcaneal fibular ligament without causing frank instability. Improper treatment and rehabilitation will lead to inadequate healing, allowing repetitive motion to cause inflammation at the ligament ends. Over time, continued activity allows the synovium to enlarge, causing impingement in the lateral gutter and chronic lateral ankle pain (Fig. 2).⁸ Hemorrhagic synovitis can occur because of mild capsule tearing resulting in hematoma formation. The hematoma eventually is resorbed by the synovium, causing synovitis. In Ferkel and Fisher’s¹² study of 31 patients with anterolateral ankle impingement, all had either hypertrophic or hemorrhagic synovitis. Subsequent studies have noted a majority of patients having synovitis present with anterolateral ankle impingement. Recently, an intraoperative classification was developed to describe impingement in the lateral gutter. This classification was based on the degree of obstruction in the lateral gutter. It ranged from normal (no abnormal soft tissue present) to severe (excessive anterolateral soft tissue preventing any visualization before shaving/debridement). In a study consisting of 41 patients with anterolateral impingement, 7 patients were noted to have what the investigators termed “synovial shelves,” which was described as a hypertrophic band of synovium extending from the anterolateral aspect of the fibula over the lateral shoulder of the talus to the anterior ankle.¹³ It has been noted that early resection of impinging synovium inhibits the progression of the cascade to chronic synovitis and scar-tissue formation.¹⁴

Fig. 2 MRI and arthroscopic view of anterolateral soft-tissue impingement. (A) Sagittal T2 demonstrating an area of intermediate signal intensity anterior to the fibula, displacing normal fat. (B) Coronal T2 demonstrates joint effusion in the lateral gutter of the talus. (C) Arthroscopic examination reveals hypertrophic synovitis causing anterolateral impingement. (D) After debridement of soft-tissue impingement.

Bassett and colleagues¹⁵ discovered another cause of impingement after inversion ankle sprains when they described the distal fascicle of the AITFL. Nikoloponlous¹⁶ originally described Bassett’s ligament in 1982 as an accessory AITFL because of the distinct fibrofatty septum between the two ligaments. The research, however, was never published in the English literature.¹⁶ The incidence of the distal fascicle of the AITFL ranges from 21% to 92%, with variation most likely caused by varying descriptions of the distal fascicle.^15–19 One investigator noted that it is most likely a common finding and only becomes pathologic after ankle mechanics become changed. The distal fascicle is found inferior and parallel to the AITFL, with its length ranging from 17 to 22 mm, a thickness of 1 to 2 mm, and width of 3 to 5 mm. An anatomic report by Ray and Kriz¹⁹ devised a classification system describing 5 distinct types (Box 1, Fig. 3).

Fig. 3 Anatomic classification system of distal anterior inferior tibiofibular ligament devised by Ray and Kriz.

(From Ray RG, Kriz BM. Anterior inferior tibiofibular ligament. Variations and relationship to the talus. J Am Podiatr Med Assoc 1991;81:482; with permission.)

The distal fascicle runs in intimate contact with the anterolateral corner of the talus. Ray and Kriz noted lateral border impingement of the talar dome in 35 of 46 specimens. In anatomic studies, associated cartilage damage is noted between 17% and 89% and has been confirmed during arthroscopic treatment.^15–19 Bassett attributed the cartilage damage as a result of increased ankle laxity from an inversion ankle sprain.¹⁵ The attenuation of the ATFL allows the anterior lateral aspect of the talus to extrude anteriorly during dorsiflexion, causing fraying of the cartilage. Akseki and colleagues¹⁸ transected the ATFL in cadavers and placed the ankle through range-of-motion testing. This process led to 4 differences where distal fascicles were already in contact with the talus in a neutral position (42 of 47 specimens).

The variation of width, length, and obliquity may also be related to pathology. Akseki determined that the mean width and length were significantly higher in fascicles that bent during dorsiflexion. It was also noted that the more distal the insertion of the fascicle near the ATFL, the more often impingement occurred.¹⁹ Bassett noted that bending of the fascicle on dorsiflexion greater than 12° might be the source of thickening and impingement. It has been noted that manual distraction of the ankle joint relieves contact and impingement of the fascicle on the talus.¹⁵ Therefore, the investigators concluded that the use of intraoperative distraction might cause the surgeon to miss a pathologic distal fascicle (Fig. 4).

Fig. 4 Arthroscopic view of AITFL with associated distal fascicle separated by fibrofatty septum.

Formation of tibiotalar osteophytes at the anterior aspect of the ankle is a common cause of chronic ankle pain.²² Anterior ankle spurring is a common occurrence in the athletic community, ranging from 45% to 60%.²³ Historically, 2 hypotheses for the etiology of anterior osteophyte formation have been described. According to McMurray,² anterior osteophyte formation develops from repeated capsular traction while having the foot in a maximally plantar-flexed position. The investigator used the example of an athlete kicking a soccer ball. Other investigators have supported this theory. However, recent anatomic studies have demonstrated this hypothesis to be unfeasible.²⁴

One cadaveric study measured the width of the non–weight-bearing tibial cartilage rim, and the distance from the tibial and talar cartilage from capsular structures were measured. The results revealed that the tibial cartilage to capsule distance was 4.3 mm and talar cartilage to capsule was 2.4 mm. The width of the tibial non–weight-bearing cartilage was 2.4 mm. This study refutes the theory that osteophyte formation is caused by traction.²⁴ Arthroscopically, tibial osteophytes are noted to be within the joint, and it is not necessary to reflect the capsule to remove the osteophyte. The cadaveric specimens were also manually manipulated to 15° dorsiflexion to study the soft-tissue components at the anterior joint space. Histopathologic analysis was performed and revealed a soft-tissue layer bordered by synovial cells forming a synovial membrane. The investigators concluded that anteriorly located soft tissue impinges between the osteophytes. This soft tissue becomes inflamed and is the source of ankle pain and not the osteophytes themselves.

The second hypothesis described by O’Donoghue,²⁵ states that the osteophytes were caused by direct trauma during forcible dorsiflexion and not at extreme plantar flexion causing traction as initially stated by McMurray. The author noted patients to have pain on end range of dorsiflexion or as the author coined “drive.”²⁵ Stoller and colleagues²³ theorized that repeated impingement causes subperiosteal hemorrhages and subsequent bone growth.

It has been noted that the non–weight-bearing anterior cartilage rim undergoes osteophytic transformation.²⁶ The investigator thought the osteophyte formation was caused by direct damage and recurrent microtrauma to the anterior cartilage rim. The same investigators performed a biomechanical analysis to determine if whether kicking a soccer ball could cause osteophyte formation by hyperplantar flexion or by direct impact.²² Results revealed that in 39% of kicking movements, maximum plantar flexion exceeded the subject’s static maximum plantar flexion. The soccer ball impact was noted at the anterior part of the medial malleolus in 76% of ball strikes, with ball velocity averaging 24.6 m/s and contact force of 1025 N. The investigators concluded that the impact location and force, not extreme plantar flexion, support the hypothesis that spur formation occurs from direct repetitive trauma to the anterior cartilage rim. This microtrauma may be compounded in patients with a history of supination injuries. A history of supination injuries has also been documented in 76% of patients with osteophyte formation in one study, and in another study the incidence of spurs was 3 times higher in an unstable ankle joint compared with a group without ankle instability.²⁷

In patients with anterolateral impingement, plain radiographs should be performed to rule out fractures, widening of the ankle mortise, or arthritic changes. Stress radiographs can be used to rule out ligament laxity. In patients with suspected anterior ankle impingement, accurate detection and localization of spurs are necessary for preoperative planning.²⁶ Standard anteroposterior and lateral views should be performed to detect anterior tibial and talar spurring. Scranton and McDermott³² devised a classification for spur formation: stage I, osteophyte less than 3 mm; stage II, osteophyte greater than 3 mm; stage III, anterior tibial osteophyte with talar osteophyte (kissing lesion); and stage IV, panarthritis. Standard lateral films have been shown to be capable of detecting only 40% of tibial and 32% of talar osteophytes. The anteromedial notch and anteromedial contour can inhibit the detection of anteromedial osteophytes.³³ Tol and colleagues³³ devised an oblique radiograph (45/30 anteromedial impingement [AMI] view) where the beam is tilted 45° in the craniocaudal direction with the leg in 30° of external rotation and the foot plantar flexed. In a study of 60 patients with anterior impingement, lateral radiographs were only able to detect lateral spurring in 58% of ankles. When detecting both tibial and talar osteophytes, the lateral view was 40% and 32% sensitive. When combined with the 45/30 AMI view, sensitivity increased to 85% and 73%.