The Pathology of Shin Splints

Transcription

1 The Pathology of Shin Splints JANET KUES, PT' The purpose of this review is to critically evaluate experimental evidence describing the pathology associated with shin splints. Shin splints are defined as medial or posteromedial leg pain which is brought about by walking, running, or related activities and which decreases with rest. The evidence indicates that shin splints may be due to pathology of the posteromedial tibia1 cortex, the periosteum of the posteromedial tibia, or the crural fascia of the deep posterior compartment of the leg. Research is needed to determine if increased pressure in the deep posterior compartment of the leg or pathology of the muscles, tendons, or interosseous membrane of the leg are associated with shin splints. Journal of Orthopaedic & Sports Physical Therapy "Shin splints" is a term commonly used to describe exercise-induced leg pain. Several areas of the leg have been cited as the focus of this pain. Among these are the posteromedial aspect of the tibia (2, 3, 7, 8, 12, 19), the anterolateral aspect of the tibia (3, 19), and the medial border of the tibia (15). Although different areas of the leg have been cited as the focus of pain, there is agreement about the nature of the symptoms associated with shin splints. The leg pain develops gradually during walking, running, or jumping (2, 4, 7-9, 11-13, 15, 19). The pain initially occurs toward the end of physical activity and decreases with rest. If the activity is continued, the intensity and duration of the pain increases and pain may even be present at rest. Most individuals will have tenderness to palpation and some may have visible swelling at the painful site (2, 4, 11, 13, 15, 19). Symptoms associated with shin splints and the types of activity which cause the pain are consistently described in the literature. There is, however, considerable disagreement concerning the pathological basis of the pain. Authors have suggested that shin splints are due to stress fractures of the tibia (4, 8, 16), myositis (3, 19-21), periostitis (2, 7, 12, 17), increased pressure in a muscular compartment of the leg (1, IS), ' Staff physical therapist. Department of Physical Therapy. Mediil College of Virginia Hospital. 401 N. 12th St.. Richmond. VA Ms Kues is currently a graduate student. Department of Physical Therapy. School of Allied Health Professions. Medical College of Virginia. V~rgln~a Commonwealth University. P.O. Box 224. MCV Station. R~chrnond. VA /90/ $02.00/0 THE JOURNAL OF ORTHOPAED~C AND SPORTS PHYSICAL THERAPY Copyright (O 1990 by The Orthopaedii and Sports Physical Therapy Sections of the American Physical Therapy Association JOSPT 12:3 September 1990 PATHOLOGY OF irritation of the interosseous membrane (14), or tendonitis (18-20). The purpose of this review is to critically evaluate experimental evidence describing the pathology associated with shin splints. In this review, shin splints are defined as medial or posteromedial leg pain which is brought about by walking, running, or related activities and which decreases with rest. Increased Pressure in the Deep Posterior Compartment of the Leg as a Possible Cause of Shin Splints Puranen (15) examined the deep posterior compartment of the legs of eight male and three female athletes who reported exercise-induced pain along the medial border of their tibias. The mean age of the athletes was 23 years (SD = 7.2 years). Six of the athletes had right leg pain, four had left leg pain, and one had bilateral leg pain. The athletes had participated in various running activities (i.e., jogging, sprinting, pole vaulting, long jumping, and hurdling) and had experienced pain for several months. Puranen stated that "conservative treatment" had failed to alleviate their symptoms. He did not define "conservative treatment." Most of the athletes in Puranen's study reported that they experienced pain only during exercise, although a few reported having pain during walking and while at rest. All of the athletes were tender to palpation along the medial border of their tibias with no signs of vascular or neurological changes. In order to eliminate stress fractures as an etiology, Puranen took radiographs and bone scans of each subject's painful leg. Two subjects SHIN SPLINTS 115

2 had periosteal thickenings along the medial border of their tibias. One subject had a significant increase in radiotracer uptake along the medial border of his tibia. Because fractures could not be seen on the radiographs of these three subjects, Puranen concluded that the subjects did not have stress fractures of their tibias. He also concluded that the subjects' pain was not of a bony origin. These conclusions may have been inappropriate. Periosteal thickening on radiographs and increased radiotracer uptake on bone scans are often the initial signs of a stress fracture (16, 21). The leg pain of the three subjects may have been due to the tibia's response to stress. Puranen incised the crural fascia of the deep posterior compartment of the involved leg in all 11 subjects. The incision was made near the insertion of the crural fascia on the medial border of the tibia. Puranen stated that in all of the subjects the fascia was "tense" and "thickened." He did not state what criteria he used to determine that the fascia was "tense" or "thickened." Puranen also visually inspected the muscles of the deep posterior compartment of each leg. According to Puranen, there appeared to be small areas of necrotic tissue in the flexor digitorum longus muscle of one subject. Although Puranen stated that a histological examination confirmed that the muscle tissue was necrotic, he did not report any of the details of this histological analysis. The crural fascia of the deep posterior compartment of the leg in all subjects was also examined histologically. Puranen removed a small portion of the crural fascia near its site of insertion on the medial border of the tibia. In nine of the subjects he found signs of "chronic inflammatory infiltration." Puranen did not describe what these signs were. Following his exploration of the deep posterior compartment of each subject's leg, Puranen left the incision in the crural fascia open and sutured the skin. After 4 weeks of rest, all of the athletes were able to return to training with complete relief of their symptoms. Based on these results and on the findings (i.e., tense and thickened fascia with inflammatory infiltration), Puranen concluded that the pain was due to the build up of excessive pressure in the deep posterior compartments during exercise. Although this explanation may be plausible, an alternate hypothesis is that the 4 weeks of rest led to relief of symptoms because the source of pain was due to bone or muscle injury. Without measuring pressure, it seems highly speculative to conclude that the athletes' pain was due to increased pressure in the deep posterior compartments. Puranen's findings suggest that pathology of the crural fascia of the deep posterior compartment may be associated with shin splints. Pura- nen did not provide evidence to support his hypothesis that an increase in pressure in the deep posterior compartment causes the pain of shin splints. Mubarak et a/. (1 3) measured the pressure in the deep posterior compartment of the legs of 7 male and 5 female subjects who had a mean age of 24.6 years (SD = 8.7 years). The subjects complained of exercise-induced pain along the posteromedial aspects of their tibias. Two of the subjects had bilateral leg pain and 10 had unilateral leg pain. Ten of the subjects were joggers, and one was a sprinter, and one a football player. Mubarak et a/. stated that the subjects' leg pain increased with weightbearing activities and decreased with rest. Weightbearing activities were not defined. Mubarak et a/. reported that each subject had tenderness over the distal one-third of their posteromedial tibias. There were no signs of motor, sensory, or circulatory changes. Radiographs and bone scans were taken of the subjects' painful legs. In 2 subjects, mild cortical hypertrophy over the medial tibias was seen. Two subjects also had mild diffuse areas of increased radiotracer uptake along the medial portion of their tibias. Mubarak et a/. used a wick catheter connected to a pressure transducer to measure the pressure in the deep posterior compartment of the legs of the subjects. Pressure measurements were taken before, during, and after exercise. Each subject exercised on an isokinetic device. The foot on the involved side was attached to the device and the subject performed dorsiflexion and plantarflexion until he fatigued or until he felt medial tibia1 pain. Apparently, the isokinetic exercise did not cause leg pain in all of the subjects. Because Mubarak et a/. appeared to be testing the hypothesis that shin splints are due to increased pressure in a muscular compartment of the leg during exercise, it would seem necessary to have the subjects perform an exercise that would cause them leg pain. The pressure measurements obtained from the deep posterior compartment of the legs of all 12 subjects, during each condition (i.e., before, during, and after exercise), were averaged and compared to average intracompartmental pressure values obtained from a group of control subjects. Details were not provided about the control subjects or about how the pressure values were obtained from these subjects. Mubarak et a/. stated that the average pressure values obtained before, during, and after exercise for the subjects with leg pain were similar to the average pressure values obtained from the control subjects. They concluded that their subjects' leg pain was not due to increased pressure in the deep posterior compartments. However, if the subjects' individual pressure measurements 116 KUES JOSPT 12:3 September 1990

3 are compared to the average control values, the conclusion may be different. Measurements obtained during exercise in three of the subjects were considerably greater than the average control value. The subjects' pressures were 125,130, and 150 mm Hg versus 60 mm Hg for the control group. According to D'Ambrosia et a/. (2), if pressure in a muscular compartment of the leg is greater than approximately 60 mm Hg, the fine intramuscular arteries will be occluded. The pressure measurements in the legs of three subjects in Mubarak et a1.k study appear to have been at pathological levels during exercise. The leg pain these subjects experienced may have been due to ischemia. The majority of the subjects in Mubarak et a1.k study appeared to have pressure measurements within normal limits. The authors, however, failed to report the reliability of their measurements. The exercise performed in this study was also not sufficient to provoke a painful episode in every subject. The results of this study, therefore, must be interpreted with caution. Mubarak et al.'s (13) findings are similar to those of D'Ambrosia et a/. (2). D'Ambrosia et a/. found no increase in the pressure of the anterior or deep posterior compartments of the legs in 14 track and field athletes who reported exerciseinduced posteromedial leg pain. Five males and 9 females with a mean age of 19.6 years (SD = 1.4 years) were the subjects. All the subjects complained of unilateral exercise-induced pain along the posteromedial aspect of their tibias. The pain increased with exercise and decreased with rest. Bone scans were taken of each subject's leg and the authors reported that there were no signs of stress fractures of the tibia. D'Ambrosia et a/. measured the pressures in the anterior and deep posterior compartments with a needle connected to a pressure transducer. The pressure in the anterior compartment of the leg was measured in all subjects. The pressure in the deep posterior compartment of three subjects' legs was measured. D'Ambrosia et a/. did not indicate why they only measured the pressure in the deep posterior compartments of three subjects. Because their subjects were complaining of posteromedial leg pain, it would have been more appropriate to measure the deep posterior compartment pressure in all subjects. The pressure measurements were also obtained with the subjects at rest. The subjects, however, experienced their pain during exercise. Methodological issues and the failure of D'Ambrosia et a/. to report the reliability of their pressure measurements bring into question their results. Summary of Pressure Studies Exercise-induced increases in pressure in the deep posterior compartment have been hypothe- sized as a cause of shin splints. An increase in pressure in the deep posterior compartment may cause pain due to ischemia. Studies, however, have failed to support this hypothesis. Stress Fractures of the Tibia as a Possible Cause of Shin Splints Devas (4) attributed exercise-induced pain along the posteromedial aspect of the tibia to stress fractures. Devas stated that out of a 'considerable number" of patients he had seen for exercise-induced leg pain, 13 males and 3 females had radiological confirmation of stress fractures. The mean age of these patients was 18.1 years (SD = 5.4 years). Fifteen of these patients had unilateral leg pain. One patient had bilateral leg pain. The patients had participated in various running sports and stated that they began to experience pain on the medial side of their legs as they were completing running. The intensity and duration of the pain was mild at first and, with continued running, increased. The pain ultimately became so severe that running could not be continued. Although the pain decreased or disappeared with rest, any running caused the pain to increase or return. The duration of the subjects' symptoms ranged from 3 weeks to 5 months. Devas reported that all 16 patients had tenderness along the medial border of their tibias and some had visible swelling in this area. In 6 patients, a localized area of subperiosteal new bone formation along the posteromedial cortex of the tibia was visible on radiographs. In the other 10 patients, an incomplete fracture extending through the posteromedial cortex of the tibia was seen on radiographs. Devas only noted radiological changes in 16 of the "considerable number" of patients he had seen for exercise-induced leg pain. He stated that all of his patients, with histories similar to those 16, had stress fractures of their tibias. He concluded that radiological changes were a late manifestation of stress fractures and that fractures would not be seen in all patients. Devas hypothesized that a stress fracture results from a series of events. He believed that with the repeated stress of running the posteromedial cortex of the tibia "disrupts" causing pain but little or no changes on radiographs. Devas believed that if the athlete rested, tibia1 changes would not progress to the point where the changes were demonstrable on a radiograph. Devas believed that if the athlete continued to run, the continued stress would lead to subperiosteal new bone formation which would be visible on radiographs. If the stress continued, a fracture of the cortex would be evident on radiographs. Stress fractures may not be immediately visible on radiographs (1 0); however, it seems spec- JOSPT 12:3 September 1990 PATHOLOGY OF SHIN SPLINTS 117

4 ulative to assume that all of the patients Devas saw (with exercise-induced leg pain and no radiological changes) had stress fractures of their tibias. The source of the leg pain may have been from nonosseous tissues. The process of stress fracture formation described by Devas was purely hypothetical and appears to have been based solely on his clinical experience. Roub et a/. (1 6) offer some evidence to support Devas' hypothesis. Roub et a/. found that some individuals with exercise-induced leg pain have localized changes in the tibia1 cortex which never progress to the point of being visible on radiographs. Roub et a/. examined 35 college athletes who had 1- to 12-week histories of exercise-induced medial leg pain. The athletes were members of track, gymnastics, or field hockey teams. Thirteen of the athletes had bilateral leg pain. According to Roub et a/., the severity of the symptoms were similar in all of the athletes. Details of the athletes' symptoms were not provided. Roub et a/. obtained radiographs and radionuclide images (bone scans) from the involved leg($ of each athlete. Athletes who exhibited no radiological changes but who had increased radiotracer uptake on the bone scan had a second radiograph taken 1 month later. A control group of 13 asymptomatic athletes from the same teams also underwent radionuclide imaging and had radiographs taken of both their legs. All subjects in the control group and six of the athletes with leg pain had no signs of stress fractures on the initial radiographs or bone scans. Details describing these subjects were not provided. On the initial bone scans, seven male and seven female athletes (15 legs) with leg pain exhibited focal, longitudinal, fusiform areas of increased radiotracer uptake along the medial cortex of their tibias. These athletes had no signs of stress fractures on the initial radiographs. However, on the radiographs taken 1 month later, there were signs of stress fractures. Roub et a/. did not state what these signs were. Four male and 12 female athletes (24 legs) with leg pain had increased radiotracer uptake along the medial border of their tibias on the initial bone scans. The pattern of radiotracer uptake in these 16 athletes ranged from focal, longitudinal, fusiform shapes to focal, vague, nondescript shapes. These athletes exhibited no signs of stress fractures on the initial radiographs or the radiographs taken 1 month later. Roub et a/., like Devas (4), believe that stress fractures form as a result of a series of events. They believe that the fractures begin microscopically and may or may not progress to the point of being radiographically demonstrable. Roub et a/. stated that a stress fracture rep resents a focal acceleration of the remodeling process in cortical bone. In the sequence of remodeling, resorption of cortical bone is followed by replacement. Osteoclastic activity resorbs bone in areas of stress and the bone is replaced by osteoblastic activity. According to the theory, when there is excessive stress, resorption proceeds rapidly and replacement is slow. During this stage of fracture formation patients complain of pain and bone scans may exhibit a slight, nondescript increase in radiotracer concentration in the area of increased stress. Radiological signs of a stress fracture will not be present. If the stress continues, resorption of cortical bone proceeds even more rapidly than replacement. During this stage of stress fracture formation, patients have pain and bone scans will exhibit a focal, intense, fusiform area of increased radiotracer concentration in the area of increased stress. Radiographic signs of a stress fracture (i.e., vague lucent cortical areas, periosteal, and endosteal thickening) will be present or will appear within a few weeks. Because at this stage the rate of resorption of cortical bone is much greater than the rate of replacement, the cortex is weakened. Periosteal and endosteal bone formation serve to reinforce the weakened cortex. A fracture that is visible on radiographs occurs only when stress causes the resorption of the cortex to be accelerated beyond the capacity of the periosteal and endosteal reactions to offer adequate support. Roub et a/. feel that appropriate treatment (e.g., rest) can allow the bone to strengthen, reversing the progression of stress fracture formation. This opinion was based on the observation that 16 of the athletes they examined had initial increases in radiotracer uptake but no radiological signs of stress fractures on the initial radiographs or the radiographs taken 1 month later. Unfortunately, Roub et a/. did not describe the activity levels these athletes maintained during this 1-month period. Furthermore, only 3 of the 16 athletes had bone scans taken 1 month after the initial scans. Radiotracer uptake was less in comparison to what was initially seen in these 3 subjects, but these findings cannot be considered representative of the other 13 athletes. Roub et al.'s findings suggest that shin splints may be due to the tibia responding to increased stress and that signs of this response may only be visible on bone scans. Unfortunately, bone scans only determine the nature of an event (i.e., increased blood flow) and not the cause. Bone seeking radiotracers concentrate in areas of increased blood flow (5, 6) regardless of the reasons for the increase in blood flow. A biopsy or some other study would be necessary to determine the actual cause of the increased blood flow. Johnell et a/. (9) biopsied the medial border KUES JOSPT l2:3 September 1990

5 of the tibia in 16 male and 4 female subjects with persistent, exercise-induced pain in this area. The mean age of the subjects was 23 years (SD = 0.5 years). One subject's pain had been provoked by rope skipping, another by calisthenics, and the others by running or jogging. Radiological changes were present in only four cases (i.e., subperiosteal new bone formation was visible). Seventeen of the subjects had bilateral leg pain. A total of 37 biopsies of the medial border of the tibias were taken. Biopsies were also obtained from the medial border of the tibia in five male and five female control subjects with a mean age of 39 years (SD = 13 years). Six of the control subjects' biopsies were taken during surgery for ankle fractures. The other four biopsies were obtained during autopsies. A soft tissue biopsy and a bone biopsy were taken from all subjects. A small portion of the crural fascia of the deep posterior compartment of the leg and a small portion of the periosteum were removed from the medial border of the tibias (soft tissue biopsy). A splinter of cortical bone was then taken from the same area. In 13 of the 37 soft tissue biopsies taken from the subjects with leg pain, Johnell et al. (9) found signs of inflammation in the crural fascia (focal aggregates of lymphocytes with histiocytes and mast cells). Only one subject had what was described as an inflammatory lesion in the periosteum. Johnell et al. described this as "plasma cell infiltration surrounding wide lymphatics." Johnell et al. failed to discuss the soft tissue biopsies taken from the control subjects. In 22 of the 37 cortical bone biopsies taken from the subjects with leg pain, Johnell etal. found signs of osteoblastic activity, vascular ingrowth, and osteoid formation. These signs were not found in any of the biopsies taken from the control subjects. Changes in the bone and soft tissue did not necessarily coincide. In 11 patients there were changes in the bone and soft tissue. In two patients there were only changes in the soft tissue and in 11 patients there were only changes in the bone. Johnell et a1.k findings indicate that pathology of the crural fascia of the deep posterior compartment and/or the cortex of the tibia may be associated with shin splints. Only four subjects had radiological signs of stress fractures (i.e., subperiosteal callus formation or sclerosis). Therefore, the authors concluded that shin splints may be due to microfractures of the tibia. Microfractures, they said, represent the first stage of a stress fracture and are not visible on radiographs. This is likely because the findings of vascular ingrowth, osteoblastic activity, and osteoid formation in 22 of the 37 cortical bone biopsies are compatible with fracture healing. Summary of Stress Fracture Studies Shin splints may be due to stress fractures of the tibia. Studies suggest that a stress fracture occurs as a result of a series of events that begin at the microscopic level and may or may not progress to radiographically demonstrable changes. The diagnosis of a stress fracture may be difficult because symptoms can develop in the absence of radiographic changes. Injuries of the Soft Tissues of the Leg as a Possible Cause of Shin Splints Several authors have hypothesized that shin splints are due to myositis and/or tendonitis of the flexor digitorum longus muscle (FDLM), the flexor hallucis longus muscle (FHLM), or the tibialis posterior muscle (TPM) (3, 19, 20, 22). Unfortunately, there have been no studies which provide evidence to support these hypotheses. Similarly, there is no evidence to support the hypothesis that shin splints are due to irritation of the interosseous membrane of the leg. One hypothesis which is supported by some experimental evidence is that shin splints are due to an inflammation or irritation of the periosteum of the tibia. Mills et a/. (12) attributed exerciseinduced pain along the posteromedial aspect of the tibia to periosteal injury at the origin of the FDLM. Mills et a/. examined one male and two female subjects who reported unilateral, exerciseinduced pain along the posteromedial aspect of their tibias. The mean age of the subjects was 17.6 years (SD = 2.3 years). Two of the subjects were runners. One subject was a football player. The subjects complained of posteromedial leg pain which they could not relate to a specific injury. Radiographs and bone scans were taken of the involved legs of the three subjects. Although there were no significant findings on the radiographs, the bone scans exhibited diffuse, linear areas of increased radiotracer uptake along the posteromedial aspect of the subjects' tibias. This pattern differed from the focal, fusiform pattern of radiotracer uptake typically seen with stress fractures (1 6). Mills et a/. (12) concluded that the areas of increased radiotracer uptake in all three subjects corresponded to the origin of the FDLM. In the pictures of the bone scans provided by Mills et al. it is apparent that each subject had a linear area of increased radiotracer uptake along the tibia. The area of increased uptake does not appear to be sufficiently discrete to relate the site to the origin of the FDLM. Therefore, Mills et al.'s conclusion is questionable. Mills et a/. hypothesized that repeated, "vigorous" contractions of the FDLM during running JOSPT 12:3 September 1990 PATHOLOGY OF SHIN SPLINTS 119

6 cause periosteal tears along the tibia. This leads to an increase in blood flow in the area and, thus, radiotracer concentration is greater in the area. Although it is generally accepted that bone seeking radiotracers concentrate in areas of increased blood flow (6), one can only hypothesize that the increase in blood flow was due to periosteal injury. The mechanism of injury may not have been solely due to contractions of the FDLM. Because several muscles of the leg are active during running, it seems unlikely that only one muscle would cause injury to the periosteum of the tibia. Mills et a/. failed to discuss why they believed that only contractions of the FDLM caused periosteal injury. Holder and Michael (7) have suggested that exercise-induced pain along the posteromedial aspect of the tibia is due to periosteal injury at the origin of the soleus muscle. They base this opinion on their evaluation of five male and five female athletes who complained of exercise-induced posteromedial leg pain. Four of the athletes had bilateral leg pain. The mean age of the athletes was 25.7 years (SD = 3.3 years). Five of the athletes were runners, two were field hockey and lacrosse players, one was a basketball player, and one was a dancer. All of the athletes had tenderness along the posteromedial border of their tibias with no signs of motor, sensory, or vascular changes in their legs. Radiographs were taken of four athletes' involved legs. No abnormalities were seen. All of the athletes underwent three-phase, radionuclide imaging of their symptomatic legs. The first two phases of the radionuclide imaging consisted of a radionuclide angiogram and blood pool imaging. These two phases were performed to determine if there was any increased vascularity of the muscles, tendons, or fascia of the leg. The third phase of the radionuclide imaging was performed to determine if there were any areas of increased blood flow in the tibia. The first two phases of the radionuclide images were normal in all of the athletes. Nine athletes (13 legs) exhibited a linear pattern of increased radiotracer uptake along the posteromedial cortex of their tibias during the third phase of radionuclide imaging. Holder and Michael (7) concluded that the athletes' leg pain was not due to myositis or tendinitis because the first two phases of the radionuclide imaging were normal. They stated that with myositis or tendinitis there is an increase in blood flow associated with inflammation. Therefore, if any of the athletes had myositis or tendinitis, the radionuclide angiogram and blood pool imaging (the first two phases of radionuclide imaging) would have been positive. Holder and Michael concluded that the tibia was the source of the athletes' pain because the third phase of the radionuclide imaging was posi- tive (i.e., increased radiotracer uptake) in 9 of the 10 athletes. More specifically, they concluded that the periosteum of the posteromedial cortex of the tibia had been injured because the pattern of increased radiotracer uptake in the athletes' tibias was diffuse and linear. Although it is likely that Holder and Michael's conclusion is correct, it would have been necessary to biopsy the periosteum of the athletes' tibias in order to verify this. Holder and Michael also concluded that, in all nine subjects, the area of increased radiotracer uptake corresponded to the origin of the soleus muscle. Although Holder and Michael found that in 9 subjects the area of increased radiotracer uptake was in the posteromedial tibia1 cortex, the portion of the tibia varied among the subjects. In some subjects, the area of increased radiotracer uptake was in the middle one-third of the tibia while in other subjects the area of increased uptake was in the upper or lower one-third of the tibia. Therefore, it is unlikely that contractions of the soleus muscle caused the periosteal injury in all of the athletes. Contractions of other muscles along the posterior aspect of the leg may have contributed to the periosteal injury. A mechanism other than muscle contraction may also have injured the periosteum. Summary of Soft Tissue Studies Bone scans of some individuals with shin splints have demonstrated a linear area of increased radiotracer uptake along the posteromedial cortex of their tibias. This pattern of increased radiotracw uptake differs from the more focal, fusiform pattern typically seen with a stress fracture. Although periosteal injury is a possible cause for the increase in radiotracer uptake, biopsies would be necessary to confirm this and to determine the exact nature of the pathology. CONCLUSION lnvasive methods, such as biopsies of the various tissues of the leg, are necessary to determine the pathology associated with shin splints. Unfortunately, these methods are impractical except in severe cases in which nonsurgical treatment has failed to relieve an individual's symptoms. Evidence from investigators that used invasive methods to determine the pathology of shin splints is limited. Existing evidence indicates that shin splints appear to be due to pathology of the posteromedial cortex of the tibia or the crural fascia of the deep posterior compartment of the leg. The three-phase radionuclide imaging de scribed by Holder and Michael (7) is a noninvasive investigatory method that appears to have some usefulness in determining the type of pathology 120 KUES JOSPT 12:3 September 1990

7 associated with shin splints. This method can be used to determine if there are areas of increased blood flow in the muscles, tendons, and bones of the leg. Assuming that a local increase in vascularity of a tissue indicates pathology, radionuclide imaging, in a subject with shin splints, can determine what tissues of the leg have been injured. The results of studies which have used radionuclide imaging suggest that pathology of the periosteum of the tibia may be associated with shin splints. Research is needed to determine if shin splints are due to exercise-induced increases in pressure in the deep posterior compartment of the leg or pathology of the muscles, tendons, or interosseous membrane of the leg. 0 The aumor would like to thank the faculty, students, and dinidans at the Medical College of Virginia who helped review this manuscript. The author would like to extend a special thanks to Jules Rothstein. PhD. PT for his input and his encouragement to get this paper published. REFERENCES 1. Benas D. Jokl P: Shin splints. Am Con Ther J D'Ambrosia RD. Zelis RF, Chuinard RO. Wtlmore J: Interstitial pressure measurements in the anterior and posterior Compartment in athletes with shin splints. Am J Sports Med 5:l DeLacerda FG: lontophoresis for treatment of shin splints. J Orthop Sports Phys Ther 3: Devas MB: Stress fractures of the tibia or 'shin soreness.' J Bone Jomt Surg (Br) 40: Genant HK. Bautovich GJ. Singh M. Lathrap K. Harper P: Bone seeking radiiudi: an in vivo study of factors affecting skeletal uptake. Radiiogy 113: Holder LE: Current concepts review. Radionudi boneimaging in the evaluation of bone pain. J Bone Joint Surg (Am) 64: Holder LE. Michael RH: The specific sdntigraphii pattern of 'shin spl~nts of the lower w. J Nucl Med Jackson SW. Bailey D: Shin splints in the young athlete: a nonspecific diagnosis. Phys Sports Med 3: Johnell 0. Raus~ng A. Wendeberg B. Westlin N: Morphological bone changes In shin splints. Cl~n Orthop 167: Matin P: Bone scintigraphy in d~agnosis and management of traumatic injury. Semin Nucl Med 13: M~chael RH. Holder LE: The soleus syndrome: a cause of medial tib~a stress (shin splints). Am J Sports Med 13: Mills GQ. Marymont JH. Murphy DA: Bone scan utilization in the different~al diagnosis of exercise-induced lower extremity pain. Clin Orthop 149: , Mubarak SJ. Gould RN. Lee YF. Schmidt DA, Hargens AR: The medial tibial stress syndrome (a cause of shin splints). Am J Sports Med 10: O'Donoghue DH: Treatment of Injuries to Athletes. Philadelphia: WB Saunders Co Puranen J: The medal tibial syndrome: exerdse ischaemia in the medial fascia1 Compartment of the leg. J Bone Joint Surg (Br) 56: Roub LW. Gummerman LW. Hanley EN. Clark MW. Goodman M. Herberl DL: B m stress: a radionud'i imaging perspective. Re diology Ryan AJ: Roundtable: leg pains in runners. Phys Spom Med 9: &he& PA: Tibialis posterior shin splint: diagnosis and treatment. Athl Train 19: Slocum DB: The shin splint syndrome: medical aspects and differential diagnosis. Am J Surg 114: Subotnik SI: Shin splint syndrome. J Am Pod Assoc 66: sweet DE. Allrnan RM: Stress fracture: RPC of the mth from AFIP. Radii , V~~tasalo JT. Kvist M: Some biomechanical aspects of the foot and ankle in athletes with and without shin splints. Am J Sports Med 11: JOSPT 12:3 September 1990 PATHOLOGY OF SHIN SPLINTS