Introduction

The structures of the posterolateral corner (PLC) are responsible for posterolateral stabilization of the knee. They resist varus angulation, posterior translation and external rotation. The PLC is a complex unit consisting of several, quite variable, structures. It is not consistently defined in the literature, and terminology is not uniformly used. Terms alternatively used for the PLC include posterolateral ligamentous complex [1] or arcuate ligament complex of the knee [2, 3]. The arcuate complex consists of the arcuate ligament (AL), fabellofibular ligament (FFL), and popliteofibular ligament (PFL) and is, therefore, more limited than other descriptions of the PLC [4]. Other authors have described three distinct layers of the posterolateral knee [4]. According to this classification, the critical structures of the PLC are those of the third or deepest layer, which includes the joint capsule, coronary ligament, FFL, popliteus tendon (PT), AL and the PFL. The lateral collateral ligament (LCL) is not among these structures. Most publications [5–10] include the LCL, the PT, the PFL, and the posterolateral capsule (including the AL and the FFL) in their definition of the PLC. This article is based on this last definition of the PLC.

An overlooked PLC injury can cause chronic pain and eventually result in osteoarthritis [11]. Missed PLC abnormalities may influence the outcome of cruciate ligament repair [2, 12, 13]. MR imaging demonstrates many structures of the PLC directly and is valuable in diagnosing PLC injuries at least based on the presence of indirect signs of abnormalities. In addition, the commonly associated injuries of the knee are demonstrated by MR imaging.

The purpose of this article is to review the anatomy, the biomechanics and the injuries of the PLC, with emphasis on MR imaging.

Anatomy and biomechanics

The anatomy of the PLC and its appearance on MR images have been demonstrated in several publications [9, 14–20]. Some structures, including the PT and LCL, have constantly been demonstrated in anatomical studies (Table 1). Others have been inconsistently visualized, both at dissection and MR imaging, including the FFL, the PFL, and the AL (Table 1). From a biomechanical point of view, the PLC primarily limits posterior translation, varus angulation and excessive external rotation [8–10]. Selective sectioning of the PLC in cadaveric specimens has been used to demonstrate the individual role of PLC structures. The PT is considered to be a dynamic stabilizer, and the LCL, FFL, PFL, and AL represent static posterolateral stabilizers [21].

Table 1 Anatomical variations and MR visualization of PLC structures [4, 6, 14–16, 20, 31, 32, 39, 82–84]
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Lateral collateral ligament

The LCL or fibular collateral ligament runs from the lateral femoral condyle to the fibular head. The proximal attachment is variable but is typically located 2 cm above the joint line, proximal and posterior to the lateral epicondyle [16, 20]. Its attachment is anterior to the insertion of the lateral gastrocnemius muscle. The LCL runs postero-inferiorly towards the fibular head. Its location is superficial. It is separated from the lateral meniscus and lateral capsule by loose connective tissue, which contains the PT and the inferior lateral genicular vessels (Fig. 1). Distally, the LCL attaches to the fibular head, anteriorly and laterally to the FFL and AL [15, 16, 20]. The LCL and the biceps femoris tendon typically form a conjoined tendon at the insertion with the LCL fibers lying deep relative to the biceps tendon fibers (Fig. 1) [14, 15]. Between the two structures, a bursa has consistently been described (the LCL–biceps femoris bursa) [16, 22]. The length of the LCL, as measured with the knee in extension, is approximately 60 mm. The mean width is 3 mm to 5 mm [14, 18, 22–25]. On routine MR examinations, the LCL is constantly visualized in normal knees (Table 1), regardless of the applied MR sequence. The normal LCL is a straight, hypointense structure (Fig. 1). Discontinuity, periligamentous signal abnormalities caused by edema or bleeding, and non-visualization are typical MR signs of abnormality.

Fig. 1
figure 1

Normal lateral collateral ligament (LCL). T1-weighted coronal (a), axial (b) images, and proton density (PD)-weighted sagittal images (c). a The normal LCL appears as a straight, hypointense structure (large white arrow). It runs from the lateral femoral epicondyle towards the fibular head (small white arrows). The ligament is superficial and is separated from the lateral meniscus by loose connective tissue which contains the popliteus tendon (PT) (large black arrow) and the inferior lateral genicular vessels (IGV) (small black arrows). The proximal insertion of the popliteus tendon (PT) (large black arrow) is lower than that of the LCL. b On the axial image just above the joint space, the LCL (large white arrow) is located anteriorly and deep to the biceps tendon (BT) (small black arrows) and superficially to the popliteus tendon (PT) (large black arrow). c Sagittal image at the level of fibular head. The LCL (large white arrow) and the biceps tendon (BT) (small black arrow) typically form a conjoined tendon

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Based on biomechanical studies [10, 18, 26–29] the LCL is a static stabiliser of the knee. During varus stress, angulation remains within normal limits so long as the LCL is intact [9]. When the LCL is sectioned and the knee is flexed, angulation increases with varus stress [9, 30]. The LCL is more important than the rest of the PLC structures in limiting varus angulation [25]. However, the LCL has limited ability to resist external rotation and posterior translation of the tibia in the flexed knee [18].

Popliteal tendon, popliteomeniscal fascicles and popliteal-fibular ligament

The PT originates from the lateral femoral condyle, from the anterior part of the popliteal sulcus, antero-inferiorly to the LCL (Fig. 1), postero-inferiorly to the lateral epicondyle, and close to the articular cartilage border [31]. At the proximal attachment two separate bundles have been described. The posterior superficial bundle is tight in extension, and the anterior deep bundle is tight in flexion [15]. Watanabe et al. [32] found such bundles along the entire course of the tendon. At the level of the femorotibial joint space, the PT is intra-articular and extrasinovial [33]. There is an extension of the synovial membrane, known as the popliteal bursa, which surrounds the tendon [34]. From here, the PT descends inferiorly and medially, runs deep to the FFL and AL and becomes extra-articular before joining the popliteal muscle, which is attached to the posteromedial surface of the proximal tibia. The PT is a constant component of the PLC. It was found in all dissected knees in cadaveric studies as well as on the corresponding MR images (Table 1) [14–16, 32, 34]. The PT is typically hypointense on all types of MR sequences (Fig. 2). Intermediate signal may be present on short TE sequences due to the magic angle effect and due to partial volume artifacts relating to its curved and oblique course. Magic angle effects most typically affect the proximal tendon on transverse MR images [14]. Partial volume artifacts are more prominent on coronal images. The use of curved multiplanar reconstruction (MPR), based on 3-D isotropic acquisitions, may improve the evaluation of the tendon by avoiding partial volume artifacts. However, to our knowledge, this statement has not formally been evaluated to date. On T2-weighted images the popliteal bursa appears as a well-circumscribed, hyperintense structure surrounding the proximal tendon. It can mimic a tear in the PT or in the posterior capsule [34].

Fig. 2
figure 2

Normal popliteal tendon (PT). Proton density-weighted sagittal image at the level of the proximal tibiofibular joint. The PT (white arrow) is typically hypointense on all types of MR sequences. Note the homogeneous fatty tissue behind the PT (black arrow). Hyperintensity on fat-suppressed T2-weighted images in this area suggests a capsular lesion

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The PT has a strong attachment to the posterior knee joint capsule, to the lateral meniscus [through the popliteomeniscal fascicles (PMFs)], and to the fibular head [through the popliteofibular ligament (PFL)]. The attachment to the posterior capsule is realized by many connecting fibres, which originate from the medial margin of the PT [15]. The two PMFs are fibrous bands that connect the posterior horn of the lateral meniscus to the popliteal synovial sheath and the posterior knee joint capsule [35]. Most authors [15, 16, 31, 32, 36, 37] describe two fascicles, although three PMFs also have been described in cadaveric knees [5, 38]. The posterosuperior PMF extends from the superomedial aspect of the popliteus tendon to the posterolateral aspect of the lateral meniscus. The antero-inferior PMF runs from the anterior margin of the popliteus tendon to the middle third of the lateral meniscus. Histologically, the antero-inferior fascicle is stronger and shorter than the posterosuperior fascicle [15, 36]. These fascicles are closely related to the popliteal hiatus. This is a constant anatomical structure (Table 1), defined medially by the body of the lateral meniscus, superiorly by the posterosuperior PMF, and inferiorly by the antero-inferior PMF [39].

The PMFs are consistently found in anatomical studies but not always on MR images (Table 1). When they are visible, the fascicles appear as hypointense bands (Fig. 3). De Smet et al. [37] have demonstrated an association between an abnormal posterosuperior PMF seen on MR images and lateral meniscal tears.

Fig. 3
figure 3

Normal popliteomeniscal fascicles (PMFs). T2-weighted turbo-spin echo (TSE) sagittal images through the lateral compartment (a, b). The posterosuperior (a) and the antero-inferior (b) PMF (arrows) are seen as low-signal intensity bands connecting the lateral meniscus to the popliteus tendon

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The PFL originates from the medial PT just proximal to the myotendinous junction and attaches to the medial fibular styloid, posteriorly to the LCL and medially and posteriorly to the insertions of the AL and FFL [40]. Three different morphologies of the PFL have been described: a single, a double, and a Y-shaped type [5, 15, 31, 38]. Based on cadaveric studies, the ligament is a strong structure with a cross-sectional area nearly as large as that of the LCL [15, 41]. The PFL has a mean length of between 10 mm and 14 mm and a mean anteroposterior diameter of 7 mm to 9 mm [5, 6, 42]. The ligament is visible as an individual structure in 90% to 100% of dissected knees [5, 6, 32, 42], but, despite its sizable diameter, its evaluation on MR images is difficult (Table 1). On MR images the ligament appears as a hypointense band-like structure located between the PT and the fibular head (Fig. 4).

Fig. 4
figure 4

Normal popliteofibular ligament (PFL). T1-weighted coronal (a) and proton density (PD)-weighted sagittal images (b). a, b The PFL (large arrows) appears as a hypointense band-like structure. a The PFL originates from the surface of the PT just proximal to the myotendinous junction (small arrow) and attaches to the medial edge of the fibular head

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The PT and popliteus muscle, the PFL and the PMF represent a functional unit that prevents posterior translation, varus angulation and excessive external rotation and which stabilizes the lateral meniscus [5, 9]. When all other posterolateral ligaments are cut, the PT and popliteus muscle still maintain neutral tibial rotation [43]. Limiting external rotation becomes more important compared to the LCL with increasing knee flexion [7]. The role of the PFL is to prevent varus angulation as well as to restrict external rotation. With a varus stress, the PFL fails after the LCL and before the PT [4]. However, by sectioning the PFL alone, no significant external rotation or varus angulation is produced. When the PT and PFL are sectioned together, external rotation at 120° flexion is increased [44].

During embryologic development, the PMFs provide vascular supply to the lateral meniscus [36]. Although, in an anatomic study [45], a strong attachment of the PMF to the lateral meniscus was not demonstrated, most papers [31, 35, 39, 46] emphasize the importance of the PMF as a stabiliser of the lateral meniscus. Moreover, injured PMFs appear to lead to lateral meniscus hypermobility and consecutive injuries [47].

Arcuate ligament and fabellofibular ligament

The AL is a Y-shaped structure closely related to the joint capsule. It has a medial and a lateral limb [1, 34]. The AL originates from the lateral edge of the styloid process of the fibula (Fig. 5) [38]. The medial limb runs superomedially, passes above the PT and attaches to the posterior knee capsule (Fig. 5). The lateral limb, which is stronger than its medial counterpart, runs vertically in close relationship with the lateral capsule and attaches to the lateral femoral condyle (Fig. 5). Occasionally, the AL may not be differentiated from the joint capsule as a separate structure (Table 1) [6, 15, 32].

Fig. 5
figure 5

Normal arcuate ligament (AL).T1-weighted coronal (a) and water-excitation true fast imaging with steady-state precession (TrueFisp) axial images (b). a The arcuate ligament (AL) originates from the lateral edge of the styloid process of the fibula. There is a medial and a lateral limb, seen as thin hypointense structures. The lateral limb runs vertically and attaches to the lateral femoral condyle (white arrow). The medial limb runs superomedially and attaches to the posterior knee capsule (black arrow). b On axial image the medial limb (large arrow) is detected superficially relative to the popliteal tendon (PT) (small arrow)

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The FFL originates proximally from the fabella and runs vertically into the lateral aspect of the fibular styloid process, anterolateral to the attachment of the PFL and posterior to the attachment of the BT [16]. Some authors [4, 25] believe that this ligament is seen only in the presence of the fabella. However, the FFL has also been described in the absence of the fabella (Fig. 6) [16, 32, 38]. In these cases the FFL attaches to the posterolateral surface of the lateral femoral condyle [32]. The reported ligament detection on dissected knees and on MR images is variable (Table 1). If present as individual structures, the normal AL and FFL may be seen as thin hypointense structures on MR images (Figs. 5, 6). The MR evaluation of the normal and abnormal appearance of these ligaments is difficult in daily clinical practice. Currently, most musculoskeletal MR examinations are performed at magnetic field strengths of 1.0 T or 1.5 T. Recently, 3.0 T MR systems have become available for clinical use, and there is preliminary evidence for improvement in detection and evaluation of small soft-tissue structures due to improved signal-to-noise ratio (SNR) [48]. It was shown that the contrast-to-noise ratios (CNRs) between different musculoskeletal structures have a potential higher at 3.0 T than at 1.5 T [49, 50]. Some authors reported improved visibility of various small anatomical structures, such as the triangular fibrocartilage complex, intercarpal cartilage and median and ulnar nerves, at 3.0 T compared to 1.5 T [49, 51, 52]. The application of parallel imaging techniques offers the opportunity of converting the additional SNR at high fields into a variety of other benefits, such as speed and resolution, and preliminary reports suggest that they may be useful for imaging the structures of the knee [53].

Fig. 6
figure 6

Normal fabellofibular ligament (FFL). T1-weighted coronal (a) and fat-suppressed proton density (PD)-weighted sagittal images (b) in two different patients. a In the absence of the fabella, the fabellofibular ligament (FFL) (large arrow) originates from the posterolateral aspect of the lateral femoral condyle (small arrow) and inserts into the lateral aspect of the fibular styloid process. b The FFL inserts into the fabella when present, (arrow)

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The AL and FFL are static stabilizers of the knee. They restrain external rotation, varus angulation and posterior translation. Selective sectioning of the LCL, PT, AL, FFL and posterior capsule results in increasing varus angulation, internal translation and external rotation. Combined sectioning of the LCL and posterior capsule, including the AL and FFL, results in an increase in external rotation at all flexion angles [21].

Posterolateral corner injuries

Injuries of the PLC are relatively uncommon when compared with other knee injuries. PLC injuries are typically combined with other injuries of the knee, such as cruciate ligament tears, meniscal tears, bone bruises and fractures, as well as soft tissues injuries. Unrecognized posterolateral injuries may be associated with chronic instability of the knee, failure of the cruciate ligaments reconstruction and osteoarthritis [2, 11–13]. By using cadaveric knees with anterior cruciate ligament (ACL) grafts, LaPrade et al. [54] have shown a statistically significant increase in force on the ACL graft during varus loading and internal rotation at different angles of knee flexion after sequential sectioning of PLC structures when they were comparing knees with ACL grafts and intact PLC structures. The results of this study demonstrate that the reconstruction of the PLC injuries is highly recommended in patients with ACL graft in order to decrease graft failure. Moreover, the reconstruction should address all of the PLC structures, since the repair of only one of the injured structures may lead to residual instability and abnormal forces in the ACL graft [54]. Other studies [55, 56] were focused on the impact of PLC injuries on the posterior cruciate ligament (PCL). In a cadaveric study [26], it has been shown that the in situ forces in PCL increased significantly in knees with PLC injuries in response to posterior tibial translation and external rotation. Mariani et al. [55], have demonstrated that the “non-healed” injuries of PCL after conservative treatment were those associated with PLC and medial collateral ligament (MCL) lesions. In their study, all six patients with associated PLC lesions showed the highest posterior instability at follow-up compared to the remaining 12 patients with PCL tear without PLC injuries.

Mechanisms of injury

PLC injuries are the result of high-energy trauma. Injury may be direct or indirect. Varus, valgus, hyperextension and external rotation forces, as well as the position of the knee during trauma, determine the extent and type of damage. A direct varus force to the anteromedial aspect of a hyperextended knee is one of the most commonly encountered mechanisms [16]. In these cases an isolated injury to the posterolateral ligaments of the knee can occur [16]. A blow to the medial tibia with the knee in variable amounts of flexion represents another direct mechanism leading to PLC injury [57]. Indirect PLC injuries can occur when the tibia is forcefully rotated externally with the knee in a varus position or when the knee is suddenly hyperextended. PLC lesions can also be found in extensive injury such as complete dislocation [58]. Contact sports (American football and soccer), traffic accidents (pedestrians), falls, and work-related accidents are the most common causes of PLC injuries [21, 57].

Associated injuries

Isolated lesions of the PLC are far less common than combined injuries. There are two different approaches to look at such combinations: (A) after the diagnosis of PLC trauma, a number of additional injuries should be specifically excluded because they are commonly associated (Table 2), and (B) there are clinical and radiological signs which should lead to specific evaluation of the PLC (Table 2).

Table 2 Lesions associated with PLC injuries
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PLC injuries are typically combined with abnormalities of the PCL (Fig. 7), the ACL, (Fig. 8), medial ligamentous structures (Fig. 9), the menisci, and bones. The diagnostic accuracy of clinical evaluation decreases as the number of lesions increases [59]. For a complete evaluation of all injuries, MR imaging is the ideal non-invasive tool. In a study by Miller et al. [60], all the patients with PLC injuries had additional injuries. Because the most typical injury mechanism is a direct varus force to the anteromedial aspect of the hyperextended knee, PCL injuries are more commonly found than ACL injuries [61]. Depending on the exact trauma mechanism, however, the ACL may also be involved (Fig. 9) [52].

Fig. 7
figure 7

Fat-suppressed T2-weighted coronal image (a), fat-suppressed proton-density-weighted axial image (b), and proton-density-weighted sagittal image (c) in a 35-year-old patient with clinical signs of PLC injuries after a car accident. a Hyperintensity (arrow) is seen throughout the popliteal musculotendinous junction. Muscle volume is increased. Perifascial fluid collections are seen. b Normal musculotendinous junction replaced by a relatively homogeneous hyperintensity (arrow). At surgery, a haematoma was found. c Associated posterior cruciate ligament tear with complete disruption and wavy contour of the remaining ligament (arrow)

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Fig. 8
figure 8

Coronal fat-suppressed T2-weighted image (a) and sagittal short-tau inversion recovery (STIR) image (b) in a 28-year-old patient with severe knee trauma. a Complete disruption of the LCL. Remaining ligament is wavy and demonstrates increased signal (large arrow). The signal changes at the proximal insertion of the PT, which is missing (small arrow) consistent with tear. b Both cruciate ligaments are torn in their middle third (arrow). At surgery, LCL, PT and both cruciate ligaments were seen to be completely torn

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Fig. 9
figure 9

Coronal fat-suppressed T2-weighted image (a) and sagittal short-tau inversion recovery (STIR) image (b) in a 28-year-old patient with popliteal tendon (PT), anterior cruciate ligament (ACL) and medial collateral ligament tear. a Hyperintensity of PT (white arrow). Non-visualization of medial collateral ligament and diffuse signal abnormality in the medial compartment (black arrow). b Bone contusion of anteromedial tibial plateau (small arrow). Tear of the distal anterior cruciate ligament (large arrow)

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Proximal LCL injuries are commonly associated with PT avulsions. Distal LCL injuries are usually combined with distal biceps tendon avulsions and meniscocapsular avulsion from the tibia [62]. Isolated PT and popliteus muscle injuries are rare. One-third of PT injuries is associated with PCL tears and bone bruises or fractures. In almost half of patients with PT injuries medial meniscal tears are found [60, 63]. Ross et al. [64] consistently found a bone contusion of the anteromedial femoral condyle in patients with PLC injuries in combination with cruciate ligaments tears. In a study by Bennett et al. [65] on 16 knees with clinically diagnosed PLC knee injuries, there were five anteromedial tibial plateau fractures or contusions seen on MR images (Fig. 9).

The “arcuate” sign is a radiographic sign which represents an avulsion of a small fragment from the proximal head of fibula [66]. Huang et al. [40] demonstrated that the bone fragment relates to the attachment of the AL, PFL, and FFL. All of their patients had clinically diagnosed posterolateral instability as well as medial collateral ligament and PCL injuries at MR imaging. The LCL was injured in half of their patients. A PT lesion was found only in one of 13 patients. In another study [1], focusing on the MR evaluation of the “arcuate” sign, tears of the cruciate ligaments were found more often (89%) than posterolateral capsule injuries (67%). Injuries of the PT and popliteus muscle were described in 33% of patients. In that study the authors described the avulsed bone fragment as the site of attachments of LCL and biceps tendon. Lee et al. [67] found that small bone fragments (1–8 mm) were the result of the avulsion of the AL, PFL, and FFL and larger (15–25 mm) fragments were the result of LCL and biceps tendon avulsion. Whenever the arcuate sign is detected on standard radiographs, MR imaging should be the next step for complete evaluation (Fig. 10).

Fig. 10
figure 10

Coronal T1-weighted image (a) and fat-suppressed T2-weighted image (b) in a 40-year-old patient with posterolateral instability. Bone avulsion from the proximal head of the fibula (large arrow) including the insertion site of the lateral collateral ligament (LCL) and biceps tendon (BT) (black arrow). Acute haematoma (small arrow) with intermediate signal intensity on the T1-weighted image (a) and high signal intensity on the fat-suppressed T2-weighted image (b). This injury pattern can typically be found when standard radiographs demonstrate the so-called arcuate sign

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The Segond fracture is an avulsion of the lateral capsule from the lateral tibial plateau [68]. This fracture is consistently associated with ACL tears (Fig. 11). However, it may also indicate an isolated PLC injury [4, 69]. Fractures of the anteromedial tibial plateau are associated with lesions of both the PLC and the PCL [70, 71].

Fig. 11
figure 11

Standard radiograph (a) and coronal short-tau inversion recovery (STIR) image (b) in a 24-year-old patient. a The radiograph demonstrates small fragment at the lateral proximal tibial plateau (arrow) representing a Segond fracture. b The MR image also demonstrates the bone fragment (large arrow), as well as signal changes in the tibial plateau (small arrow) and adjacent soft tissue

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Clinical evaluation

Clinical symptoms depend on a number of factors. In the acute phase there may be pain and swelling over the posterolateral corner, but, commonly, these symptoms are minimal [72]. Motor weakness in the foot is present when the common peroneal nerve is injured. In the chronic phase, a feeling of discomfort may persist at the PLC. Patients may complain about instability of the knee in hyperextension, noticed when climbing or descending stairs. During physical examination, posterolateral rotatory instability can be present (posterior subluxation of the lateral tibial plateau on external rotatory movements) [72]. Different clinical tests are used for diagnosing PLC injuries. The posterolateral drawer test and external rotation recuvatum test described by Hughston et al. [73] are most accurate. However, the findings of the clinical tests can be difficult to interpret [1] and may be of limited value in the acute phase, due to pain and swelling. Early diagnosis is valuable because surgical reconstruction improves clinical outcome if performed during the first 3 weeks of injury [2, 74–77]. An anatomical repair or refixation of the different posterolateral structures in patients with high varus instability showed a statistical significant improvement at follow-up. In a study by Baker et al. [76], of 13 patients who were operated on for acute posterolateral instability, none required additional treatment at follow-up. Moreover, in most of the cases (85%), the patients returned to normal athletic activity. The treatment choice and the surgery results are influenced by the extent (complete or incomplete tear) and the location of the injury. A differentiation between a musculotendinous popliteal lesion and an avulsion of the tendon is difficult at clinical examination, yet the surgical options for these lesions are different [41]. The presence or absence of associated abnormalities also influences the postoperative outcome. Some authors reported an effective reconstruction in patients with isolated PLC [41] injuries, with no failure at 2.5 years’ follow-up. In the case of multiligament-associated lesions the treatment is more difficult, and complete motion reacquisition is not always achieved [41]. Arthroscopy is valuable in the evaluation of acute injuries and for evaluation of associated meniscal and cartilage abnormalities in chronic PLC damage [21, 31, 57]. Arthroscopy does not demonstrate all injuries of the PLC, however, and may worsen capsular damage in the acute phase due to the fluid extravasation [11].

MR findings

Magnetic resonance imaging potentially demonstrates the entire spectrum of PLC injuries and associated lesions of the knee, including those that might be overlooked during clinical examination and arthroscopy. The MR diagnosis of PLC abnormalities is based on the same criteria as those used for any tendon, ligament, or muscle.

A partial tear of the LCL or PFL may be indirectly recognized on MR images by the accompanying soft tissue edema and bleeding (Fig. 12). The ligaments are in continuity but are often thinned or thickened [60]. Fat-suppressed T2-weighted images are useful for the diagnosis. Complete disruption, with or without waviness of the remaining ligament, typically associated with hyperintensity on fluid-sensitive sequences within and around the lesion, indicate a complete tear (Fig. 8). Inhomogeneous signal intensity within the ligaments may be seen in both partial or complete tears. A partial tear of the musculotendinous junction of the PT is seen as an amorphous or feathery signal abnormality of the muscle belly, extending into the tendon, without or with muscle defect (Fig. 13) [60]. The feathery changes are the result of interstitial edema and haemorrhage [78, 79]. A complete discontinuity of the musculotendinous junction with tendon retraction indicates a complete tear. When a hematoma is present, enlarged muscle volume and perifascial fluid collections are frequently seen (Fig. 8). Short-tau inversion recovery (STIR) and frequency-selective fat-suppressed T2-weighted sequences are the best sequences for this diagnosis. By using these criteria, MR imaging is an accurate tool in the diagnosis of LCL, PT and popliteal muscle injuries. Although the majority of PT lesions are located extra-articularly at the myotendinous junction [63], avulsion of the femoral insertion of PT, as well as intra-articular tears, is not unusual (Fig. 10). PMF tears may also be seen on MR images directly but are also diagnosed when the fascicles are no longer seen [37]. De Smet et al. [37] suggested that an abnormal posterosuperior PMF is significantly associated with lateral meniscal tears. In their study the posterosuperior PMF was abnormal in nine of the 30 patients with lateral meniscal tear and were normal in all 29 patients with a normal meniscus. Simonian et al. [47] have demonstrated intrameniscal abnormality and knee locking in three patients with isolated PMF lesions.

Fig. 12
figure 12

Coronal, fat-suppressed, T2-weighted (a) and T1-weighted (b) images in a 55-year-old patient with partial lateral collateral ligament (LCL) tear after varus injury. Soft-tissue edema surrounds the proximal part of the LCL (arrow)

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Fig. 13
figure 13

Sagittal fat-suppressed T2-weighted image in a 45-year-old patient with partial tear of the popliteal musculotendinous junction (arrow)

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Injuries of the posterior capsule structures, including the AL and FFL, may not be directly seen on MR images but should be suspected in the presence of surrounding soft tissue edema and hemorrhage (Fig. 14) [80]. Signal abnormalities may be present anteriorly, posteriorly, or on both sides of the capsule [37]. Normally, there is homogeneous fat tissue behind the PT (Fig. 2) Hyperintensity seen on T2-weighted images posterior to the PT suggests a capsular tear. Individual assessment of the integrity of the AL, PFL, and FFL may not be possible [40].

Fig. 14
figure 14

Sagittal fat-suppressed T2-weighted (a), axial fat-suppressed T2-weighted image (b), and coronal proton-density-weighted images (c) in an 18-year-old patient with pain at the posterolateral corner after a fall. Signal abnormalities (a–c) are seen on both sides of the capsule (large arrow). A small haematoma is also seen (small arrow) (a, b). Injuries of arcuate ligament (AL) and fabellofibular ligament (FFL) should be suspected

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MR imaging appears to be useful in assessing the PLC. In a large series of knees (n = 481) Miller et al. [60] have demonstrated that, although in only three patients PLC injuries were clinically suspected, MR imaging identified 30 patients in whom at least one of the PLC structures was involved. Twaddle et al. [81] were able to correctly assess 82% of LCL injuries on MR images. During the clinical evaluation, only 71% of the lesions were diagnosed. Other authors [40, 58] have reported an accurate diagnostic of LCL injuries in 100% of cases. Yu et al. [58] demonstrated that PT abnormalities were detected in seven of eight patients with arthroscopically proven lesions.

Conclusions

PLC injuries are not very common. If present, they are associated with injuries of the cruciate ligaments and other internal derangements of the knee in a majority of cases. The choice of treatment and the clinical outcome are influenced by an early correct diagnosis. An overlooked injury can result in chronic pain, chronic instability, and degenerative changes of the knee. Although the complex anatomy and the variability of PLC structures are a challenge for diagnosis, MR imaging is a valuable tool in assessing PLC injuries and associated abnormalities, especially because the clinical diagnosis can be challenging.