Exercise-induced chronic leg pain is a common condition in compet itive and recreational athletes. By definition, lower leg pain is pain between the knee and ankle [1, 2]. The causes of chronic lower leg pain in the athlete are numerous, and therefore the differential diagnosis is quite broad (Appendix 1).

According to the literature, despite the wide range of potential diagnoses, medial tibial stress syndrome and stress fractures are the most common sources of exercise-induced chronic lower leg pain, followed by chronic exertional compartment syndrome and popliteal nerve entrapment [1–4].

Although a high index of suspicion, careful physical examination, and detailed history are essential in athletes with chronic lower leg pain [1–3], “even for an astute clinician, distinction between the different medical causes may be difficult given that many of their presenting features overlap” [5]. Consequently, the role of diagnostic imaging remains fundamental in detecting the cause of chronic lower leg pain.

The objectives of this article are to describe the imaging features in athletes with chronic lower leg pain, emphasizing the roles of MRI and CT, which are the diagnostic tools with the highest sensitivity and specificity in the differential diagnosis of lower leg pain [5, 6], and to propose a diagnostic algorithm in patients with chronic lower leg pain.

Tibial stress injuries are by far the most common cause of lower leg pain in athletes, accounting for up to 75% of exertional leg pain [7]. Tibial stress injuries include various types of bone lesions that represent a continuum of abnormalities from asymptomatic osteopenia to fracture, all occurring in response to abnormal repetitive stress applied to normal bone [5–7]. This spectrum of lesions includes periostitis, cortical osteopenia, cancellous bone, and cortical fractures, often associated with various degrees of reactive soft-tissue and bone marrow edema [5–7]. Although both proximal and distal metaphyses and the whole diaphysis can be involved by stress injuries, such injuries more frequently occur in the cortex of the distal two thirds of the tibia and cause a clinical syndrome known as medial tibial stress syndrome or shin splints.

Periostitis can occur both as an isolated abnormality or in association with bone stress injuries. Although a bone scan can be positive in this condition, MRI is the most sensitive examination for diagnosing periostitis [5]. Periostitis appears as a soft-tissue edema near the cortex. Often, on STIR or fat-saturated T2-weighted images, detached periosteum can be seen as a thin hypointensity surrounded by hyperintense edema (Fig. 1A, 1B).

Cortical lesions include osteopenia, cavitations, striations, and fractures. Radiog raphy detects only a small number of cortical fractures. The other cortical abnormalities and the majority of cortical fractures (up to 94%) remain undetected [8] (Fig. 2A, 2B, 2C). Both MRI and CT have high accuracy in detecting the spectrum of cortical abnormalities. MRI is the most sensitive single diagnostic tool for patients with medial tibial stress syndrome given its excellent soft-tissue contrast to show soft-tissue abnormalities [5] (Figs. 3A, 3B and 4A, 4B). However, sometimes CT permits the early diagnosis of cortical abnormalities not visible on MRI [6] (Fig. 5A, 5B).

Chronic exertional compartment syndrome is a cause for claudication in athletes. It is caused by abnormally increased pressure within muscular compartments that are enclosed by relatively noncompliant fasciae. Of the four lower leg muscular compartments, anterior and lateral compartments are affected more frequently than others (76%), followed by deep posterior (16%) and posterior superficial (12%) [9].

The diagnosis of chronic exertional compartment syndrome requires measuring compartment pressure with a slit or weak catheter. However, some problems exist: Pressure measurement is an invasive technique. Potential risks include muscular hernia or neurovascular damage [9]. Multiple compart ments are affected in about half of chronic compartment syndrome cases and symptoms in the bilateral legs occur in approximately 75% of cases [10]. Chronic exertional compartment syndrome may be complicated by the coexistence of periostitis and tibial stress fracture, which cannot be diagnosed by compartment pressure measurement.

MRI is a promising technique for non-invasive diagnosis of chronic exertional compartment syndrome [11, 12]. A recent work has shown that the sensitivity of MRI in diagnosing chronic exertional compartment syndrome was comparable to that of intracompartmental pressure measurement and near-infrared spectroscopy [11].

MRI must be performed immediately after exercise-inducing pain. MRI findings in chronic exertional compartment syn drome include muscular hyperintensity on T2-weighted or fast STIR images with or without muscular swelling (Figs. 6 and 7). Inhomogeneous hyperintensity within affected compartments can be seen (Fig. 6). MRI may detect involvement of more than one compartment (Fig. 6) and concurrence of medial tibial stress syndrome.

Further studies are necessary to define the appropriate role of MRI in the diagnostic algorithm of chronic exertional compartment syndrome. In the meantime, MRI should be used as a problem-solving examination in confusing circumstances, in patients refusing compartment pressure measurement, or in patients with contraindication for compartment pressure measurement (coagulation disorders).

Compression or nerve entrapment can lead to a functional disturbance or pathologic change in the peripheral nerve of the lower leg causing lower leg pain and muscular dysfunction. The superficial peroneal nerve and sural nerve can be involved, but the most common cause of extraspinal neuropathic leg pain is common peroneal nerve disease, which can be caused by trauma, compression, and intrinsic abnormalities.

Although the diagnosis of common peroneal nerve injury is based initially on electromyography, MRI plays an important complementary role in diagnosing the cause of the nerve sufferance [13]. Moreover, MRI can also show muscular neurogenic edema in the subacute phase and atrophy with fatty degeneration in the chronic phase of denervation [14] (Fig. 8A, 8B).

Muscular neurogenic edema appears on fast STIR and fat-saturated T2-weighted turbo spin-echo images as a diffuse homogeneous hyperintensity involving the muscles innervated by diseased nerve. Hyperintensity of denervated muscles is usually seen after 2–3 weeks but can appear as early as 4 days after acute traumatic denervation [14]. Muscular neurogenic atrophy with fatty infiltration due to long-standing denervation is well shown by T1weighted MR images. This is important clinical information because neurogenic atrophy is irreversible damage.

Popliteal artery disease is an uncommon cause of intermittent claudication of the lower leg in young athletes. The most common cause (up to 60%) is popliteal artery entrapment syndrome, which typically occurs in young men [15–17]. This syndrome is caused by anomalous musculature in the popliteal fossa, in which the popliteal artery is entrapped [15, 16] (Fig. 9A, 9B, 9C, 9D). Popliteal artery entrapment syndrome may be complicated by thrombosis [15] (Fig. 9A, 9B, 9C, 9D). Other rarer causes of intermittent claudication in young athletes are adventitial cystic disease, muscular fibrodysplasia, arteritis, and compression of the artery by exostosis of the distal femur [17].

The diagnosis of popliteal artery dis ease requires not only depiction of arterial stenosis but also identification of the responsible disease. Although arterial stenosis can be shown on conventional angiography and sonography, CT and MRI are equally better in showing the cause of popliteal abnormalities [15–17] (Fig. 9A, 9B, 9C, 9D). However, MRI has some advantages over CT, including lack of ionizing radiation and the need for contrast material as well as higher soft-tissue contrast [16].

Among the uncommon causes of chronic lower leg pain in athletes, a number of soft-tissue and bone diseases should be considered, including tumors and infection [1–3], tendinopathy of the proximal Achilles tendon (Fig. 10A, 10B), other more unusual tendinopathies (Fig. 11A, 11B), interosseous membrane injuries, and chronic bursitis (Fig. 12A, 12B).

We propose a diagnostic algorithm for differential diagnosis in athletes with chronic lower leg pain (Fig. 13). It is useful to remember that, according to Edwards et al. [2], the first diagnostic step is always represented by radiography. The advantages of radiography are low cost, short imaging time, and easy execution. Radiography has a low sensitivity but may reveal tibial stress fractures, bone tumors, and soft-tissue calcification (calcific tendinitis, calcific soft-tissue tumors, and so on). CT and MRI may be useful to better evaluate the abnormalities shown by radiography.

Address correspondence to S. Mazziotti ([email protected]).