Since the first reports in 1975 [13], the number of cases of chronic compartment syndrome due to prolonged exercise – running, hiking, roller skating, motocross, wind surfing [14] – has dramatically increased.

An increase in intratissue pressure within a compartment enclosed in an unyielding fascia defines the condition. Ischemia can be the ultimate result. There is normally an intricate balance between capillary pressure, intratissue pressure, venous pressure, and osmotic protein pressure. Muscular contraction is normally associated with an inflow of water into the muscle. If the compartment is abnormally tight or the contraction excessively intense, the pressure within the muscle rises to abnormally high values during relaxation, causing symptoms. This is probably an oversimplification of the pathophysiology of chronic compartment syndrome. In a muscle biopsy study, Wallensten [15] found that patients had higher percentages of slow fibers with a high oxydative potential, hypotrophy of the same fibers, and decreased production of lactic acid, compared with the controls. However, these abnormalities could be either causes or consequences of the compartment syndrome. The most frequent compartment syndromes concern the lower leg, divided into three muscular compartments, one antero-lateral, one deep posterior, and one superficial posterior [16]. Involvement of the antero-lateral compartment is common in all published studies, whereas involvement of the superficial posterior compartment is rare and consistently accompanied with involvement of the deep posterior compartment. But all compartments can be concerned, in particular the forearm and the foot.

Pain is the main symptom. It is usually confined to the involved compartment and initially occurs at a given level of activity, although the interval to occurrence of pain tends to decrease over time. Fullness of the compartment upon palpation is common. These manifestations resolve completely within an average of ten minutes with rest.

Patients with antero-lateral compartment syndrome sometimes have one or several muscular herniations, transient foot-drop, or sensory loss in the territory of the superficial fibular nerve.

Intramuscular pressures at rest and at cessation of the activity that induces the symptoms should be measured to confirm the diagnosis. The measurement technique was first described by Whitesides [14]. A number of devices for intramuscular pressure measurement are now available, including the Stic Catheter (Stryker Instruments) that provides fast, highly reproducible results. Pressures do not normally exceed 15 mmHg at rest and 30 mmHg (25 mmHg for forearm) after exertion. While patients with chronic compartment syndrome often have normal basal values, their values after exertion are abnormally high and return to normal levels only after several minutes.

Because intramuscular pressure measurement remains an invasive procedure, MRI has been proposed as an alternative for diagnosis. Numerous studies have shown an increase in T1 and T2 relaxation time in muscles involved in compartment syndrome [17–21]. In a study of 13 military recruits, Eskelin has shown an excellent correlation between the increase of intracompartmental pressures and MR signal intensity on T2-weighted images at rest and after standard dynamic exercise on a treadmill (Fig. 9.2) [17]. This technique requires, however, the use of parameters that are sensitive to muscle water content. As absolute values of signal intensity may be hindered by technical factors such as field inhomogeneity, the author suggests better accuracy from normalized values using ratios of T2 signal intensity compared to subcutaneous fat, tibial bone marrow or superficial posterior compartment muscles. As an example, when tibial bone marrow was used as the normalization tissue, the increase in T2 signal measurement was 24 % ±2 in the control group and 98 % in symptomatic patients with more than 40 mmHg pressure on manometry [17]. Similarly, with the use of fasciotomy as the gold standard, Verleisdonk et al. have shown an increase in the signal intensity ratio between anterior and posterior superficial compartments of 21 % (12.2–32 %) after exercise, with values of 3.9 % and −1.8 % in the control and post fasciotomy groups, respectively [18]. More recently, Litwiller et al. have proposed improving the technique by promoting an in-scanner exercise added to a novel dual birdcage coil. An in-scanner exercise device means the patient can exercise and stress the muscles without getting in and out of the machine [19]. This technique drastically shortens the delay between exercise and acquisition of images, thus limiting the risk of false negatives since signal modifications related to exercise are known to fade in a few minutes. Concurrently, the use of a dedicated dual birdcage allows reduced field inhomogeneity and increases signal to noise ratio. In that study, a threshold of 1.54 for the ratio of relative T2-weighted signal intensity increase compared to baseline offered a sensitivity of 96 %, specificity of 90 % and accuracy of 96 % [19, 20]. Development of such a technique may nevertheless be limited to medical care structures with a high volume of patients with chronic compartment syndromes.

Compartment syndromes in the forearm were studied in a population of motocross racers. That study, using MRI, found the flexor digitorum superficialis and profundus to be predominantly involved [21].

Rare acute exertional compartment syndromes have been reported in the literature [22, 23]. In an emergency, MRI may demonstrate edema in all of the fibers of the involved muscle, thus confirming the diagnosis in the absence of any reported trauma [22]. In a case that required urgent surgery of the adductor muscles, signal intensity was found to be normal four months postoperatively while the normal fiber structure required additional months to return to normal [23].

Surgical fasciotomy is the only way to resolve symptoms and avoid progression towards acute compartment syndrome. Rorabeck [24] has described the surgical procedure for each compartment. Patients should refrain from athletic activities for one month after the procedure. Most can resume activities at the presurgical level at the end of the second postoperative month.

Variant muscles include accessory muscles, hypertrophy of normal muscles, abnormal trajectory of muscles and abnormal organization in transverse or longitudinal planes of muscles.

An accessory muscle is a supernumerary structure that shares some similarities, especially of trajectory, with a normally existing one from which it usually inherits its name. While the frequent presence of accessory muscles has long been reported in anatomic studies [23], exertion-related leg pain caused by these muscles is a recently and infrequently identified condition. Awareness of this syndrome is important to avoid errors in diagnosis and treatment. Most subjects, however, have an accessory muscle, an abnormality whose embryology and phylogeny have been extensively studied by Gordon [25]. Patients are invariably young adults who engage in sports (running, ball games, motor bicycle, wind surfing) several times a week and who experience heaviness or cramping pain in the muscle compartment upon exertion. The pain resolves in few minutes with rest. We have observed this pathology in many cases, for forearm, thigh, leg and foot. Examination after exercise can, in some cases, demonstrate swelling, which sometimes fluctuates upon palpation but hardens during contraction of the muscle. The swelling is present in both legs in more than half the patients. At rest we can observe local hypertrophy, in particular during contraction of the involved muscle.

An accessory soleus is one of the most typical example of accessory muscle in the lower leg. Proximally, the muscle inserts on the soleal line of the tibia and fibula in the lower third of the leg to reach the distal end of the calcaneal tendon or the upper or medial edge of the calcaneal bone [25, 26] (Figs. 9.3 and 9.4). Distal insertion of the muscle can be fully muscular or through a thin tendon [26–28]. Such details can be accurately depicted with ultrasound or MRI that confirm its typical muscular appearance and explore its relationship to neighboring structures [26]. An accessory soleus usually partly fills up a wide amount of the Kager fat pad [29, 30]. MRI is also especially efficient in differentiating this variant muscle from others that may lie in the posteromedial ankle, namely the flexor digitorum accessorius longus (FDAL) and tibiocalcaneal internus muscles [30]. On axial T1-weighted images, the accessory soleus remains posterior and superficial to the flexor retinaculum and reaches the calcaneus. Conversely, the FDAL is located anteriorly to the retinaculum and posteriorly to the flexor hallucis longus tendon to insert onto the flexor digitorum longus distally (Figs. 9.5 and 9.6) [30]. Due to this position, the FDAL lies in close vicinity with the posterior tibial neurovascular bundle. If PCI and FDAL may be confused because both travel anteriorly to the flexor retinaculum, the latter differentiates itself by the fact it lies laterally to the flexor hallucis longus, travelling with the latter through the calcaneal groove to insert onto a small tubercule beneath the sustentaculum tali, on the medial aspect of the anterior calcaneus [30].

An accessory soleus may have multiple clinical presentations, including the vast majority of pathophysiologic ways from which a variant muscle can become symptomatic (Table 9.1). Mass effect related to the muscle may clinically raise the suspicion of a tumoral lump and require exploration with imaging [30]. As mentioned earlier, the muscle may bulge and occupy an anatomical space that is usually free of any mass effect, leading to a compartment-like syndrome. In contrast with transient modifications of signal encountered in compartment syndromes, the fact that modifications of signal on T2-weighted images are sometimes encountered demonstrates the occurrence of muscular strain within the muscle [26]. This may result, in some cases, from the inadaptation of the muscle to mechanical stress. Finally, close proximity of the accessory muscle and neurovascular bundle may lead to tunnel syndrome. In a study of 18 athletes, Kinoshita showed variant muscles to impinge on the posterior tibial nerve in four cases, including three FDAL and one accessory soleus [31]. Two other possible complications of accessory muscles, that to date have not been reported with the accessory soleus, may occur in the ankle in the vicinity of an accessory muscle. Snapping of the peroneus tertius is reported when impinging with the lateral talar dome during flexion-extension of the ankle [32]. Tenosynovitis of a flexor hallucis longus is reported when impinging on an FDAL [33, 34] or peroneocalcaneus internus muscle [34].