Journal Logo

Original Articles

Medial tibial stress syndrome

KORTEBEIN, PATRICK M.; KAUFMAN, KENTON R.; BASFORD, JEFFREY R.; STUART, MICHAEL J.

Author Information
Medicine & Science in Sports & Exercise: March 2000 - Volume 32 - Issue - p S27-S33
  • Free

Medial tibial stress syndrome (MTSS) is one of the most common causes of exercise related leg pain (5,38). Originally coined by Drez and reported by Mubarak et al. in 1982 (31), the term describes a specific overuse injury producing increasing pain along the posteromedial aspect of the distal two-thirds of the tibia (27,31). Although runners are most commonly afflicted, with one study reporting a 13% incidence (14), individuals involved in jumping activities may also develop this disorder (13). The term “shin splints” is frequently used synonymously with this disorder (29,38); however, as advocated previously (5,13,25), this term should be abandoned, and MTSS used instead, since it more aptly describes the location and presumptive etiology of this disorder.

HISTORY/TERMINOLOGY

In 1958 Devas initially suggested tibial stress fractures as a cause of shin soreness (17), and stress fractures are now characterized as a very common cause of exertional leg pain. In addition, over the past decades several other causes for this pain have been characterized. These include chronic compartment syndromes (most frequently of the anterior and deep posterior compartments), entrapment of arteries (popliteal or external iliac) or nerves (superficial peroneal nerve), deep vein thromboses, rupture of the gastrocnemius muscle, fascial herniations, and muscle strains (38). Simple muscle strains are probably the most common cause of acute exercise induced leg pain, while more subacute or chronic pain may be caused by stress fractures or chronic (exertional) compartment syndrome (CCS) (13). Patients with exertional medial tibia pain remain a diagnostic challenge. Although progress has been made over the past several decades and rational etiologic theories exist, there continues to be considerable confusion and controversy regarding the most appropriate terminology to be applied to these patients. This is most likely because neither a specific pathologic mechanism nor a discrete pathologic abnormality has been identified in these patients. Although this review includes several well controlled studies completed recently, the reader should realize that this review is based primarily on collected case studies, expert opinion, and theory.

Over the past 30 years many appellations have been introduced, including generic terms such as “medial tibial stress syndrome,” “medial tibial syndrome,” “tibial stress syndrome,” and “shin splints” (15,31,33,40), as well as terms meant to infer a specific anatomic or pathologic aberration, such as “posterior tibial syndrome,” “soleus syndrome,” and “periostitis” (22,29,31). Of all these terms, medial tibial stress syndrome is the most appropriate (5,13,25) since there are distinct drawbacks to each of the others that are addressed in this review.

Shin splints has been the most problematic term since it is the least descriptive and thus the most confusing. While most authors recommend dropping it from the medical lexicon (5,13,25), others have advocated its continued use (9). Although the specific origins of the term are not precisely known, it was apparently originally a lay term that became a medical diagnosis through common usage (40). Since it had no formal definition, and thus was used rather imprecisely by both the public and the sports community (40), a subcommittee of the American Medical Association (AMA) was tasked with formulating a definition. In 1966 the AMA publication The Standard Nomenclature of Athletic Injuries defined shin splints as a “pain or discomfort in the leg from repetitive running on hard surfaces or forcible, excessive use of the foot flexors; diagnosis should be limited to musculotendinous inflammations, excluding fracture or ischemic disorder” (34,40).

Slocum commented over 30 years ago that in light of this rather specific definition shin splints should no longer be considered a catchall diagnosis for any condition causing pain in the lower leg after exertion (40). Despite this admonition, shin splints continues to be used to describe almost any type of exertional leg pain. As recently as 1995, shin splints was defined as inclusive of chronic compartment syndrome and stress fracture (3), and more recently, it was noted to be “a nonspecific term used to describe exertional lower leg pain from almost any cause” (4).

This continued confusion most certainly persists since shin splints does not implicitly refer to any specific location or infer an etiology for the pain associated with this syndrome. Since the AMA definition does not explicitly specify any particular location, some authors have limited the location of pain to the distal medial tibia (11,22,31,33,43,45), while others include patients with either medial or proximal anterolateral tibia pain (2,8,9,40).

Due to dissatisfaction with the term shin splints, several other terms have been suggested. These include “medial tibial syndrome,” “tibial stress syndrome,” “posterior tibial syndrome,” “soleus syndrome,” and “periostitis.” While these terms may arguably be an improvement, each has its limitations, either because of inadequate supportive evidence or because of possible misinterpretation of the terminology as initially reported.

Puranen introduced medial tibial syndrome (32) in 1974, after noting excellent results in 11 patients with chronic exertional medial tibia pain who had had a posteromedial fasciotomy. From these observations he suggested that the pain resulted from ischemia of the deep flexor compartment muscles during prolonged exercise. However, subsequent studies (31,45) in similar patients have not demonstrated abnormal compartment pressure elevations. In the same year Clement (14) theorized that tibial stress syndrome was the clinical prologue to the development of a stress fracture. He hypothesized that during exercise the shock absorbing function of the lower leg muscles is eventually impaired secondary to muscle fatigue, resulting in greater stress transmission to the bone and an eventual stress fracture. Since the clinical presentation, response to treatment, and radiological findings of these two disorders are quite different (37), it is unlikely that chronic MTSS is a precursor to a stress fracture. As will be discussed, individuals with more acute MTSS may eventually develop a stress fracture, as suggested by Batt (9).

In 1978 James et al. (23), explicitly noting dissatisfaction with the imprecise, nonspecific meaning of shin splints, suggested posterior tibial syndrome as an alternative, since the origin of the tibialis posterior muscle was thought to be the source of the pain. This is unlikely, however, since subsequent anatomic studies (11,29) have demonstrated that this muscle has a more lateral tibial origin. Several years later, the term “soleus syndrome” was proposed (29). These authors had noted a distinctive pattern of increased uptake on triple phase radionuclide bone scan in individuals with characteristic exercise induced medial leg pain. The location of the uptake appeared to coincide with the origin of the medial soleus muscle. However, this terminology is probably too specific, since more recent anatomic studies have not been able to exclude other deep flexor compartment muscles from consideration (11,18). Finally, when Mubarak et al. (31) initially introduced Drezs’ term, they suggested periostitis as the essential etiology of MTSS, which was subsequently supported by several authors (5,13,27). This term is probably inaccurate as well since scintigraphic and biopsy studies indicate that this disorder is probably not an inflammatory process of the periosteum (2,4,9,16,24,31,33). In fact, while a true inflammatory process would demonstrate increased uptake on the first two phases (angiogram and blood pool) of a triple phase bone scan (20,21), the most frequent finding in these patients is diffuse uptake on only the delayed (third) phase of the scan (22,29,37). This finding is more indicative of bone remodeling (20). In addition, several studies have reported the results of pathologic examinations of periosteum, fascia, and bone biopsied at the time of fasciotomy in recalcitrant cases of MTSS (2,16,24,29,31,33). These studies represent a total of over 75 biopsy samples. Of all these specimens only four have documented evidence of periostitis (2,29,31). Of note, a substantial number (22 of 75) of these biopsies demonstrate evidence of fascial inflammation, most commonly of the crural fascia (31,33), and an equal number show increased vascular ingrowth, increased numbers of osteoblasts, and osteoid, indicative of enhanced bone metabolism (24 of 75).

Further confusing the terminology, in 1986 Detmer proposed a tripartite classification system for chronic MTSS (14). According to this schema, stress fractures or bone stress reactions are categorized as a type I lesion, periostalgia caused by avulsion of the tibial periosteum near the fascial insertion of the soleus is a type II lesion, and chronic compartment syndrome of the deep posterior compartment is a type III lesion. As noted by Clanton (13), however, this is only a clinical stratagem since each of these disorders may be differentiated with a thorough clinical evaluation and appropriate laboratory studies (7,13). It is also interesting to note that while Detmer noted periosteal avulsion with adipose tissue interposed between the bone and periosteum at fasciotomy in a majority of his patients with the Type II disorder, these findings have not been replicated in any previous or subsequent studies. Finally, although not explicitly mentioned, this system may cause further confusion since it tends to imply a progression in severity of a single pathophysiological mechanism despite any supportive evidence to this effect. Thus this schema is not recommended (13) and is not generally used.

As discussed above, there are problems with each of the aforementioned terms that preclude any particular one being used exclusively for this disorder. However, a single terminology to describe this would be extremely helpful in further defining the specific characteristics of this group of patients, as well as for performing multistudy analysis (9). This would aid in the determination of predisposing risk factors, the efficacy of different treatment regimens, and hopefully the identification of the etiological mechanism and the specific pathologic abnormality. While MTSS may not be the perfect terminology, it is the most appropriate term for these patients at the present time, since it describes the location and probable pathophysiology of this disorder.

EPIDEMIOLOGY

Because of the varied and inconsistent terminology, it has been difficult to determine a precise incidence or frequency for MTSS. In a short-term prospective study, Andrish et al. (6) reported an incidence of 4.1% during a summer training program for students entering the U.S. Naval Academy, while Clement et al. (15) in a retrospective review identified 239 cases out of 1819 total injuries (1650 patients) for an incidence of 13.2%. As previously noted, runners are most commonly afflicted, although individuals involved in jumping activities, such as basketball, volleyball, or long jumping, may also develop MTSS (5,13). In addition, there does not appear to be any predilection to one gender versus the other.

ETIOLOGY

While neither the precise pathophysiologic mechanism nor the specific pathologic lesion in MTSS is known, the anatomic site of the abnormality has been fairly well localized. Initial conjecture, as noted previously, implicated the tibialis posterior muscle; however, recent information has identified the fascial insertion of the medial soleus as the most probable source (11,29). As previously described, Holder and Michael (22) reported a characteristic abnormality on triple phase bone scan in several patients with complaints of chronic (mean 12.6 months) posteromedial tibia pain. Specifically, these subjects demonstrated low grade uptake of the radiotracer along a diffuse region of the posteromedial tibia only on the delayed phase of the scan. Subsequent anatomic dissections on cadavers, as well as EMG and muscle stimulation studies by this same group, provided further confirmatory evidence that this area of uptake coincided with the origin of the medial soleus muscle, and its deep fascial insertion, termed the “soleus bridge” (29). Beck and Osternig (11) examined the tibial attachment sites of the soleus, flexor digitorum longus, and tibialis posterior muscles, as well as the deep crural fascia in 50 cadaver legs. They found that while the insertions of the soleus muscle and the deep crural fascia were most consistently attached to the posteromedial aspect of the distal two-thirds of the tibia, consistent with the previous findings, the flexor digitorum longus (FDL) muscle was also noted to insert in this region although less frequently. These authors considered the tibialis posterior muscle a less likely source since its origin tended to be located more laterally on the tibia. Thus, while it appears that the origin of the medial soleus is the most likely source of pain in these patients, the FDL cannot be excluded.

While running, the foot initially makes contact with the ground in a relatively supinated position and moves into a relatively more pronated posture as the foot progresses through the stance phase. Since the soleus is the primary plantarflexor and invertor of the foot (12), Michael and Holder theorized that the medial portion of this muscle must contract eccentrically as the foot moves from relative supination to pronation (29). Accordingly, this results in increased stress of the fascial origin of the medial soleus, possibly disrupting the Sharpey’s fibers that traverse through the periosteum to insert in the fibrocartilaginous bone of the tibia (29,37). This remains the most well accepted theory regarding the etiology of MTSS (5,9). Although the FDL has also been implicated as a possible source of pain because of its anatomic location, it is not specifically known whether, or how, this muscle is affected.

Some differentiation should be made between acute and chronic MTSS (9). The pathophysiology of those individuals developing characteristic symptoms after a brief exposure to high intensity training, such as in a military boot camp setting, are most assuredly different from the recreational or competitive athlete enduring or developing symptoms after several years of training. It has been theorized that individuals with relatively acute symptoms may proceed in at least two directions (9). If sufficient rest is interspersed with continuation of the inciting activity, appropriate adaptation of the tendons, fascial insertions, and bone may result despite the continued stress. Alternatively, an inadequate or inappropriate adaptation of these structures resulting from excessive stress or insufficient rest may result in a stress fracture, fasciitis, or tendonosis (9). Evidence from a recent study (4) that evaluated subjects with characteristic exertional medial tibia pain using magnetic resonance imaging (MRI) appears to support this theory. These authors reported that individuals with relatively shorter duration symptoms (mean 10 months) were more likely to have abnormal MR findings than those with more chronic symptoms (mean 46 months). Although the precise pathologic abnormality has not been identified, it appears to involve a stress reaction by the crural fascia (fasciitis) or bone along the posteromedial portion of the tibia (38) and probably not the periosteum (13,24). It is conceivable that acutely there is both fascial and bone stress, and as suggested by Batt (9), some may go on to develop a (traction) fasciitis while others may develop a stress fracture. This theory, however, probably does not explain the pathophysiology of the chronic disorder.

It should also be recognized that these individuals may present with two disorders concurrently, such as MTSS and chronic compartment syndrome (16,38). In addition, a second disorder may result from an alteration in gait mechanics resulting from pain from the initial problem (9,16).

BIOMECHANICS

Clinical observations have noted excessive foot pronation to be a risk factor for MTSS, and this has been supported by several biomechanical analyses (28,41,44). Viitisalo and Kvist (44) examined 35 patients with a history of MTSS, as well as 13 normal runners with high-speed cinematography, and found that the individuals with MTSS did indeed have a greater degree of pronation than the control subjects. These individuals also had greater standing Achilles tendon angle measures as well. Messier and Pittala (28) also compared a group of individuals with MTSS with a group of control subjects using high-speed cinematography, as well as with anthropomorphic measures such as leg length discrepancy, Q angle, ankle range of motion, and hamstring and leg flexibility. While they also noted that maximum pronation was significant in the subjects with MTSS, the maximum velocity of pronation was even more significant in these individuals. Another study (41) has also found more pronounced varus fore- and hindfoot abnormalities in a group of these individuals, as well as evidence of a greater degree of standing foot pronation.

PRESENTATION

The most common complaint in these patients is a dull aching pain along the middle or distal posteromedial tibia (5,9,13,18,27,30,31,33). Early in this process, the pain may occur at the beginning of a run, resolve with continued exertion, only to recur toward the end or after a workout (5,27). Alternatively, the pain may only be noted toward the end of a run (18,30). At this early stage, the pain typically subsides promptly with rest (5,13,30). With continued training the pain may become more severe, sharp, and persistent (5,13,27). Patients may attempt trials of complete rest only to have the pain recur with resumption of training. With increasing chronicity, the pain may be present with ambulation or at rest (5,13,27). Complaints of dysesthesias or ischemic pain are not typically present either during or after exercise.

Training errors have been reported to be causative in approximately 60% of these cases (18,25). Most commonly symptoms occur after a relatively abrupt increase in the frequency, duration, or intensity of training (e.g., increase of over 30% of initial training mileage within 1 yr) (5,18,23). Excessive hill training, as well as changes in training surface, or worn out footwear have also been implicated (18,23,25,27).

Patients with either stress fracture or chronic compartment syndrome (CCS) often present somewhat differently; however, there may be considerable overlap. Individuals with stress fractures most commonly complain of the insidious onset of pain and tenderness of a very focal region of the tibia that progressively intensifies with continued training (5,26,42). Often the pain may be persistent throughout the day, and night pain may be present as well. Subjects with CCS usually develop a tightness and discomfort of the muscles of the involved compartment after running for a specified distance or duration (5,13,38). Their pain usually resolves relatively promptly, typically within 5–15 min, after stopping exercise (5,13,38). These patients may also note a cramping sensation or numbness of the distal extremity in the region of distribution of the nerve traversing the involved compartment (5,13,38).

PHYSICAL EXAMINATION

In virtually every patient with MTSS there is a diffuse region of tenderness along the posteromedial edge of the tibia (5,13,27,31) (Table 1). Usually this involves the middle and distal thirds of the tibia, from approximately 12 cm proximal to the medial malleolus extending distally to about 4 cm proximal (5). Infrequently there is palpable edema or warmth of this same region, or pain with percussion of the tibia (5,13,18). A less consistent finding in patients with MTSS is discomfort with contraction or stretching of the plantarflexor (soleus) musculature (5,7). Progressive loading of this muscle group may be performed with the following maneuvers (Table 2): forced passive dorsiflexion, active plantarflexion against resistance, two-leg standing toe raises, one-leg standing toe raises (23), two-leg standing jump or hop, and maximal stress may be elicited with a one-legged hop (14).

Table 1
Table 1:
Typical physical examination findings in MTSS, stress fracture, and chronic compartment syndrome.
Table 2
Table 2:
Provocative testing for MTSS or stress fracture.

These physical exam findings should be contrasted with the findings of a typical stress fracture (Table 1) in which there is a discrete location of tenderness with palpation. Frequently there is well localized pain at this same site with percussion, as well as with bony percussion distant from that location. Conversely, individuals with chronic compartment syndrome usually have a completely normal exam, and discomfort may only be reproduced by performing the inciting activity. Alternatively, specifically exercising the muscles of the involved compartment (5,13) may reproduce the pain. With exercise, muscle weakness or dysesthesias in the area corresponding to the nerve traversing the compartment may be noted. The neurovascular examination is normal in patients with MTSS as well as in those with stress fractures or chronic compartment syndrome except as noted above.

Careful evaluation for foot pronation or subtalar varus should also be performed. Passive subtalar motion may be measured in the prone position on the examination table. Viitasalo and Kvist (44) reported greater motion in their subjects with MTSS (20° inversion, 10° eversion) compared with controls (14° inversion, 8° eversion). However, another study reported that 27° was the normal range of motion for both varus and valgus (35). A standing foot angle (the angle between the medial malleolus-navicular prominence and the navicular-first metatarsal segment) less than 140° has also been associated with MTSS (40). Dynamic measures of rearfoot motion, as noted before, may be more sensitive measurements of MTSS (28,44), although they require high-speed cinematographic equipment as well as trained personnel.

IMAGING

Plain radiographs in patients with MTSS are almost universally interpreted as normal (5,13,27,29) (Table 3). Rarely there is posterior cortical hypertrophy noted, consistent with a periosteal reaction to the increased repetitive bony stress (5). If abnormalities such as periosteal thickening, subperiosteal lucencym, or scalloping are seen, a tibial stress fracture should be ruled out with serial x-rays, a bone scan, or possibly a CT scan (5,13).

Table 3
Table 3:
Characteristic laboratory findings in MTSS, stress fracture, and CCS.

A triple phase bone scan is particularly useful in differentiating MTSS from a stress fracture (Fig. 1) and virtually assures the diagnosis when the classic diffuse longitudinal region of uptake is noted along the posteromedial aspect of the tibia only on the delayed phase of the scan (4,5,13,18,29,37). Medial and lateral views are suggested to localize the region of uptake more precisely (5,21,29). Tomographic bone scans (SPECT views) may help identify more difficult lesions.

Figure 1
Figure 1:
Triple phase radionuclide bone scans of MTSS and a tibial stress fracture for comparison. Oblique views of the legs demonstrate a focal area of uptake in the distal tibia (left), while the other leg demonstrates a more diffuse low grade area of uptake consistent with MTSS.

Two recent studies have reported the use of MRI in the evaluation of this disorder. Fredericson et al. (18) studied 14 runners with 18 symptomatic lower limbs. Each subject complained of characteristic exertional leg pain and had bone scan evidence of MTSS, a tibial stress reaction or stress fracture. MR imaging was performed on each symptomatic leg and correlated with the findings on bone scan. In 14 of the 18 (78%) subjects, the MRI findings correlated with the findings on scintigraphy. However, since the MRI findings of the patients with symptoms and bone scan findings consistent with MTSS were not differentiated from those with stress reaction or fracture, this study is not particularly helpful in delineating the specific MRI findings associated with MTSS. These authors also noted diffuse abnormalities adjacent to the insertion of all the deep flexor compartment muscles. Anderson et al. (4) performed MRI on 19 patients with symptoms and physical exam findings consistent with MTSS. This subject group had more chronic symptoms with a mean duration of 24 months compared with a mean of 10 months in the Fredericson (18) study. In this study, seven subjects had normal MR images, five had evidence of periosteal fluid usually of the medial anterior tibia, five had bone marrow edema (two also had periosteal fluid), and two had stress fractures. Bone scans for correlation were not performed, and only five subjects had x-rays (all negative). In four of the five with periosteal fluid, the fluid was noted to extend toward the insertion of the medial soleus. Since correlative bone scans were not performed, it is not known whether similar results could have been obtained with this technique. As previously mentioned, these authors noted an inverse relationship between the MR findings and the duration of symptoms. As noted by the authors, this may be an indication that two distinct pathophysiological mechanisms are responsible for the acute and chronic presentations of this disorder.

TREATMENT

Initial management of MTSS primarily entails some type of “relative” rest of the involved extremity (5,13,18,27,30). Specifically, the inciting activity, most commonly running, should either be avoided or the training volume decreased transiently. Any other pain provoking activities should be avoided as well. Activity modification may be delayed temporarily depending on the patient’s desire to complete a competitive season, although the potential for developing a coexistent stress fracture should be considered and discussed with the patient. In addition, the patient should understand that the alteration in running gait mechanics may be sufficient to induce the development of another overuse injury. If pain is present with normal walking or at rest, crutches may be used to eliminate all weight bearing. This should be continued until the patient is pain free, typically within a few days.

Cross-training exercises, such as swimming, cycling, or water running, are recommended for the patients desiring to maintain their cardiorespiratory fitness (5,18,27). Again, if pain occurs with any of these activities, for instance, with ankle plantarflexion while cycling, that exercise should be avoided until it may be performed without any discomfort. Water running, if available, may be the most beneficial non-weight-bearing activity, since runners can maintain their aerobic conditioning and running efficiency (46).

Cryotherapy with ice massage should be instituted for at least several days since it may provide some benefit (5,18). Numerous other rehabilitation modalities are often recommended, including ultrasound, phonopheresis, cortisone injections, bone electrical stimulation, and acupuncture; however, none have been definitively demonstrated to be efficacious (5,10,18). Maintaining adequate calcium intake and ensuring females have appropriate estrogen levels also appear to be important (10). If analgesia is required, acetaminophen or nonsteroidal anti-inflammatory drugs (NSAID) may be recommended. Since MTSS appears not to be an inflammatory disorder, the routine use of NSAID does not appear to be warranted. While heel cord stretching has not been demonstrated to be an effective prophylactic measure in at least one study (6), it is often recommended after MTSS has developed (5,13,18). Stretching should be done with the knee fully extended, as well as in a partially flexed position, since in the latter position a more isolated stretch of the soleus muscle occurs.

If anthropomorphic malalignment is noted, the patient should be referred for fabrication of orthotics (5,13,18). A medial forefoot post may be useful for a forefoot varus deformity, while a heel post may be beneficial for excessive pronation (5). In one recent study the use of standard shoe insoles were noted to decrease the incidence of MTSS in a military boot camp population (39), whereas a previous study with heel inserts demonstrated no effect (6).

After the patient has been pain free for several days, walking, or light running may be started (5,18). The patient is advised to begin training at approximately 50% of the previous intensity and distance (duration) (5) on soft, level surfaces. In addition, the patient should warm-up thoroughly and stretch before each training session and cool down and stretch again after each workout. Gradually, training distance or duration may be increased as long as the individual remains asymptomatic. It is generally recommended that these parameters may be increased approximately 10% per week so that the original training duration or distance is achieved in 3–6 wk (5). Training may be increased more rapidly as long as the patient remains pain free; however, this increases the chance of recurrence. Training intensity should only be increased after progression in the distance or duration. There are no studies evaluating this graduated rehabilitation regimen although the results are generally felt to be quite good (5). Eventually plyometric exercises may also be recommended (18). If symptoms recur at any time during this progression, the patient should again rest for several days after resolution of the pain (5). Training, possibly starting at a lower intensity or duration, or alternating several minutes of walking with running, is then gradually reintroduced.

Fasciotomy of the posteromedial superficial and deep fascia of the tibia is an option in patients with chronic recalcitrant symptoms that have failed several attempts with conservative measures. This procedure is thought to alleviate the pull of the soleus and the deep compartment muscles on their fascial insertions (13). In addition, it has been suggested that this may result in denervation of the periosteum (45). Detmer (16) has reported a success rate of greater than 90% at 6 months follow-up with his technique, which included cautery of the tibial periosteum, while Holen et al. (19) reported that 78% of their patients were improved 16 months after fasciotomy.

Athletes and coaches should also be aware of measures that may prevent MTSS, including ensuring adequate strength and flexibility of the triceps surae musculature, correction of improper running technique, changing footwear every 300–400 training miles, and adhering to an appropriately graduated training program (10).

CONCLUSION

Although multiple terms have been used for patients with diffuse exertional medial tibia pain, in particular, the term “shin splints” has been most confusing. Despite being defined quite specifically over 30 years ago, this term continues to be used indiscriminately to describe any type of exertional leg pain. The term “medial tibial stress syndrome” (MTSS) is most appropriate since it most aptly describes the location, and the presumptive etiology of this disorder. The use of consistent terminology will aid in the investigation of specific risk factors, pathophysiological mechanisms, diagnostic studies, and treatment of this syndrome. The etiology and pathogenesis of this syndrome are not definitively known; however, excessive stress at the fascial insertion of the medial soleus or flexor digitorum longus muscles appears to be most likely. This syndrome may be diagnosed clinically since the symptoms and physical findings in these patients are quite characteristic. A triple phase bone scan is useful in differentiating MTSS from stress fracture since each has a distinctive scintigraphic pattern. The majority of these patients can expect to return to their previous levels of activities after a graduated rehabilitation program, although fasciotomy may infrequently be necessary in some recalcitrant cases.

The authors express appreciation to Thomas Beckman, M.D., for a critical review of this manuscript.

REFERENCES

1. Allen, M. J. and M. R. Barnes. Exercise pain in the lower leg: chronic compartment syndrome and medial tibial syndrome. J. Bone Joint Surg. 68B:818–823, 1986.
    2. Allen, M. J., F. G. O’Dwyer, M. R. Barnes, I. P. Belton, and D. B. Finlay. The value of 99Tcm-MDP bone scans in young patients with exercise-induced lower leg pain. Nucl. Med. Comm. 16:88–91, 1995.
    3. Amendola, A., C. Rorabeck, D. Vellett, W. Vezina, B. Rutt, and L. Nott. The use of MRI in exertional compartment syndromes. Am. J. Sports Med. 18:29–34, 1990.
    4. Anderson, M. W., V. Ugalde, M. Batt, and J. Gacayan. Shin splints: MR appearance in a preliminary study. Radiology 204:177–180, 1997.
    5. Andrish, J. T. Leg pain. In: Orthopedic Sports Medicine, J. C. DeLee and D. Drez (Eds.). Philadelphia: W.B. Saunders, 1994, pp. 1603–1607.
    6. Andrish, J. T., J. A. Bergfeld, and J. Walheim. A prospective study on the management of shin splints. J. Bone Joint Surg. 56A:1697–1700, 1974.
    7. Barry, N. N. and J. L. McGuire. Acute injuries and specific problems in adult athletes. Rheum. Dis. Clin. North Am. 22:540–541, 1996.
    8. Bates, P. Shin splints: a literature review. Br. J. Sports Med. 19:132–137, 1985.
    9. Batt, M. E. Shin Splints: a review of terminology. Clin. J. Sports Med. 5:53–57, 1995.
    10. Beck, B. R. Tibial stress injuries. Sports Med. 26:265–279, 1998.
    11. Beck, B. R. and L. R. Osternig. Medial tibial stress syndrome: the location of muscles in the leg in relation to symptoms. J. Bone Joint Surg. 76A:1057–1061, 1994.
    12. Campbell, K. M., N. C. Biggs, P. L. Blanton, et al. EMG investigations of the relative activity among four components of the triceps surae. Am. J. Phys. Med. 52:30–41, 1973.
    13. Clanton, T. O. and B. W. Solcher. Chronic leg pain in the athlete. Clin. Sports Med. 13:749–751,.
    14. Clement, D. B. Tibial stress syndrome in athletes. J. Sports Med. 2:81–85, 1974.
    15. Clement, D. B., J. E. Taunton, G. W. Swart, and K. L. McNicol. A survey of overuse running injuries. Physician Sportsmed. 9:47–58, 1981.
    16. Detmer, D. E. Chronic shin splints. Sports Med. 3:436–446, 1986.
    17. Devas, M. B. Stress fractures of the tibia in athletes or “shin soreness.” J. Bone Joint Surg. 40B:227–239, 1958.
    18. Fredericson, M., A. G. Bergman, K. L. Hoffman, and M. S. Dillingham. Tibial stress reaction in runners. Am. J. Sports Med. 23:472–481, 1995.
    19. Holen, K. J., L. Engebretsen, T. Grontvedt, I. Rossvoll, S. Hammer, and V. Stolz. Surgical treatment of medial tibial stress syndrome(shin splint) by fasciotomy of the superficial posterior compartment of the leg. Scand. J. Med. Sci. Sports 5:40–43, 1995.
    20. Holder, L. E. Clinical radionuclide bone imaging. Radiology 176:607–614, 1990.
    21. Holder, L. E. Radionuclide imaging in the evaluation of bone pain. J. Bone Joint Surg. 64A:1391–1393, 1982.
    22. Holder, L. E. and R. H. Michael. The specific scintigraphic pattern of “shin splints in the lower leg”: concise communication. J. Nucl. Med. 25:865–869, 1984.
    23. James, S. L., B. T. Bates, and L. R. Osternig. Injuries to runners. Am. J. Sports Med. 6:40–50, 1978.
    24. Johnell, O., A. Ransing, B. Wendelberg, and N. Westlin. Morphological bone changes in shin splints. Clin. Orthop. 167:180–184, 1982.
    25. Jones, D. C. and S. L. James. Overuse injuries of the lower extremity: shin splints, ITB friction syndrome, and exertional compartment syndromes. Clin. Sports Med. 6:273–290, 1987.
    26. Knapp, T. P. and W. E. Garrett. Stress fractures: general concepts. Clin. Sports Med. 16:346, 1997.
    27. Krivickas, L. S. Anatomical factors associated with overuse sport injuries. Sports. Med. 24:140–141, 1997.
    28. Messier, S. P. and K. A. Pittala. Etiologic factors associated with selected running injuries. Med. Sci. Sports Exerc. 20:501–505, 1988.
    29. Michael, R. H. and L. E. Holder. The soleus syndrome: a cause of medial tibial stress (shin splints). Am. J. Sports Med. 13:87–94, 1985.
    30. Moore, M. P. Shin splints: diagnosis, management, and prevention. Postgrad. Med. 83:199–210, 1988.
    31. Mubarak, S. T., R. N. Gould, Y. F. Lee, D. A. Schmidt, and A. R. Hargens. The medial tibial stress syndrome (a cause of shin splints). Am. J. Sports Med. 10:201–205, 1982.
    32. Pedowitz, R., A. Hargens, S. Mubarak, and D. Gershuni. Modified criteria for the objective diagnosis of chronic compartment syndrome of the leg. Am. J. Sports Med. 18:35–40, 1990.
    33. Puranen, J. The medial tibial syndrome. J. Bone Joint Surg. 56B:712–715, 1974.
    34. Rachun, A., F. L. Allman, M. E. Blazina, D. L. Cooper, R. C. Schneider, and K. S. Clarke. Standard Nomenclature of Athletic Injuries. Chicago: Am. Med. Assoc., 1966, p. 126.
    35. Roaas, A. and G. B. J. Andersson. Normal range of motion of the hip, knee, and ankle joints in male subjects, 30–40 years of age. Acta Orthop. Scand. 53:205–208, 1992.
    36. Rorabeck, C., R. Bourne, P. Fowler, J. Finlay, and L. Nott. The role of tissue pressure measurement in diagnosing chronic anterior compartment syndrome. Am. J. Sports Med. 16:143–146, 1988.
    37. Rupani, H. D., L. E. Holder, D. A. Espinola, and S. I. Engin. Three phase radionuclide bone imaging in sports medicine. Radiology 156:191, 1985.
    38. Schon, L. C., D. E. Baxter, and T. O. Clanton. Chronic exercise induced leg pain in active people. Physician Sportsmed. 20:100–114, 1992.
    39. Schwellnus, M. P., G. Jordaan, and T. D. Noakes. Prevention of common overuse injuries by the use of shock absorbing insoles: a prospective study. Am. J. Sports Med. 18:636–41, 1990.
    40. Slocum, D. B. The shin splint syndrome. Am. J. Surg. 114:875–881, 1967.
    41. Sommer, H. M. and S. W. Vallentyne. Effect of foot posture on the incidence of medial tibial stress syndrome. Med. Sci. Sports Exerc. 27:800–804, 1995.
    42. Stanitski, C., J. McMaster, and P. Scranton. On the nature of stress fractures. Am. J. Sports Med. 6:391–396, 1978.
    43. Styf, J. Diagnosis of exercise-induced pain in the anterior aspect of the lower leg. Am. J. Sports Med. 16:165–169, 1988.
    44. Viitasalo, J. T. and M. Kvist. Some biomechanical aspects of the foot and ankle in athletes with and without shin splints. Am. J. Sports Med. 11:125–130, 1983.
    45. Walensten, R. Results of fasciotomy in patients with medial tibial syndrome or chronic anterior compartment syndrome. J. Bone Joint Surg. 65A:1252–55, 1983.
    46. Wilber, R. L., R. J. Moffatt, B. E. Scott, D. T. Lee, and N. A. Cucuzzo. Influence of water run training on the maintenance of aerobic performance. Med. Sci. Sports Exerc. 28:1056–1062, 1996.
    Keywords:

    SHIN SPLINTS; CHRONIC COMPARTMENT SYNDROMES; STRESS FRACTURE; PERIOSTITIS MUSCLE STRAIN

    ©2000The American College of Sports Medicine