Zone Of Confusion: Diagnosing Tendinopathy In the Plantar Midfoot
Tendinitis, The Term That Needs To Die
Tendinopathy is now the term of choice for the clinical condition following overuse injury. The terms tendinosis and tendinitis are histopathological descriptions and should not be used without microscopic confirmation. Overuse tendon injuries cause pain, reduce strength and function, and decrease tolerance and length of exercise. The Achilles tendon and posterior tibial tendon are among the most common areas affected by tendinopathy in runners.
Surgical specimens taken from patients with well-established tendinopathy show little to no signs of inflammation. Instead, the specimens show hypercellularity, an increase in proteoglycan content, vascularization, and a loss of the usual tightly bundled collagen appearance. Tendinopathic tissue is usually grey or brown in color. Physically the tissue is soft and fragile. Animal preparations do not demonstrate inflammation as a component of long standing tendon injury. Inflammation is only seen in cases of acute and extreme tendon loading. The microscopic pathology of both mid-tendon and enthesis injuries is histologically similar. Repetitive overload and microtrauma can occur in conjunction with non-uniform stress within a tendon. The result is local fiber degeneration. A single abnormal loading cycle (e.g. a misstep) could be enough to create isolated fibril damage. The patient would not likely recall a specific injury. Neer believed impingement could be a cause of tendinopathy in the supraspinatus tendon below the anterior margin of the acromium. (Neer 1983) An analogous process may contribute to peroneus longus tendinopathy adjacent to the cuboid bone.
Tendon overload creates matrix changes in the collagen structure. There is an increase in proteoglycans, and cellular protein and enzyme production is altered. Production of prostaglandin E2 and leukotriene B4 are increased. These compounds likely contribute to the development of tendinopathy. Apoptosis may also play a role. An increase in cytochrome-c related caspace activation is a potential inductive pathway for apoptosis. Heat shock protein (HSP-25) is also found in animal models of tendinopathy with apoptosis. (Xu and Murrell 2008)
Theories of Tendon Pathology
We need to look at other possible mechanisms for overuse tendinopathy, as inflammation is no longer believed to be the major cause. The features described above are all compatible with the current major theories of tendinopathy. The theory of incomplete healing views the injured tendon as being in a healing phase, with active cellular activity and increased protein production occurring in the midst of a disorganized matrix and neovascularization. This has also been termed “failed healing”. (Iglehart 2006)
Overuse tendon injuries have also been viewed as a degenerative process. The terms hypoxic degeneration, mucoid degeneration or hyaline degeneration are often applied. This suggests an end stage and difficult to reverse process. (Jozsa and Kannus 1997) It is possible that a continuum may exist with incomplete healing leading ultimately to a degenerative process. Cook and Purdam have described this hypothesis. (Cook and Purdam 2009)
Magnetic resonance imaging (MRI) and diagnostic ultrasound (US) are the most frequently employed diagnostic procedures. In contrast to tenography, both of these procedures are non-invasive and cause no further to damage to the tissues. US is a fast and inexpensive technique which can be performed in an office setting. Tendon thickening, echogenic changes around the tendon, and adhesions are readily seen. Tendons affected by tendinosis, on US examination, show low reflectivity peripherally. In chronic tendinosis, peritendinous adhesions are seen as a hypoechoic paratenon with poorly defined borders. MRI using relatively small spaced images provide greater detail, but takes longer to perform and is considerably more expensive.
Clinical examination is still an important component of the evaluative process. Bains and Porter (2006) state that “clinical evaluation remains the main criterion measure” for evaluation of potential areas of tendinopathy. (Bains 2006)
Zone of Confusion: Re-evaluating Intractable Plantar Fasciitis
In this zone, too many injuries are often called “plantar fasciitis.” At the lateral corner of the “zone of confusion” injuries to the cuboid, os peroneum, peroneus longus are often misdiagnosed as the nebulous “cuboid syndrome”. Also in this "zone of confusion" there are several midfoot tendons that are often injured but not considered in the diagnostic process. We will pay special attention to the peroneus longus tendon and the flexor hallucis longus tendon. These two tendons along with the insertion of the posterior tibial tendon and the mid portion of the plantar fascia, sit in what I call in this article the “zone of confusion”. A high level of suspicion combined with careful examination should lead to the proper diagnosis. Treatment failure often follows a failure to make the correct diagnosis. Diligence in creating a reasonable set of differential diagnoses should be done for each patient. Careful examination, consideration, and imaging when necessary will minimize diagnostic errors.
The plantar midfoot can be an area of consternation. Classically, the midfoot includes the navicular, cuboid and the three cuneiform bones. It lies anterior to Choparts joint which includes the calcaneocuboid and talonavicular joints. Our zone of confusion extends within the soft tissue a bit distal to this. Many times pain in this area is mistakenly ascribed to plantar fasciitis or plantar fasciopathy. Perform a painstakingly careful evaluation of this area while keeping in mind the structures you are palpating. Specifically, trace and palpate the Peroneus longus tendon, flexor hallucis longus tendon, and the insertion point of the posterior tibial tendon. Any of these tendons could cause symptoms that mimic plantar fasciopathy. We’ll focus on these clinical entities, but you should keep in mind more dorsal structures that could contribute to pain in this area including: Lisfrank ligament or joint injury, metatarsal stress fracture, cuboid stress fracture, navicular stress fracture, and plantar fascia tear.
Zone of Confusion
P.T.–Insertion of posterior tibial tendon.
P.L.–Peroneus longus tendon. F.H.L–Flexor hallucis longus tendon
Structures Affected In The Zone of Confusion
Posterior Tibial Tendon/Spring Ligament
The posterior tibial tendon (PTT) runs behind the medial malleolus in a fibro-osseous groove and inserts primarily into the navicular tuberosity but also into the cuneiform bones. In the athletic population overtraining and excessive pronation of the foot are risk factors. MRI can be an adjunct to diagnosis and to recognition of tears in the tendon. The spring ligament (plantar calcaneonavicular ligament) is a static structure, but functions in tandem with the posterior tibial tendon. An injury to the spring ligament would usually be found only in conjunction with an injury to the PTT. The MRI would show the ligament to be abnormally thickened and would demonstrate an increased signal intensity. Previous articles have discussed posterior tibial tendon dysfunction in detail.
Accessory Navicular Bone
The accessory navicular bone is reported to occur in up to 21% of the population. This bone may slightly increase the risk for PTT pathology. Type I accessory navicular bones are small, round, and can be located considerably proximally. They have the appearance of a sesamoid bone and are not likely to create any dysfunction in the PTT. Type II accessory navicular is larger and sits immediately adjacent to the main body of the navicular bone. Type II accessory navicular bones are what most clinicians readily observe. Type III navicular bone is cornuate shaped and incorporates the accessory navicular into the body of the navicular. An injured accessory navicular bone (Type II) will show bone marrow edema and possibly cyst formation. PTT pathology can often be seen in conjunction with the injury to the accessory navicular bone. (Ting, Morrison et al. 2008)
Os Peroneum/Peroneus Longus Tendinopathy
The os peroneum is a sesamoid bone found within the peroneus longus tendon. It is usually located just proximal to the cuboid tunnel. This bone is thought to be present in the majority of people and a corresponding facet is found in the cuboid 93% of the time. The os peroneum is often only partly ossified or fibrocartilagenous. It is visible on x-ray only 5% of the time.
In conjunction with an inversion injury and tenderness at the cuboid the os peroneum is often a contributing factor in lateral foot pain. This bone can traumatically fracture. In the presence of a painful os peroneum the MRI often shows signs of tendinopathy of the peroneus longus tendon, along with peritendinopathy, and bone marrow edema of the cuboid. (Sobel M 1994) Sclerosis and fragmentation of the os peroneum after chronic pain have also been found.
Clinically, always examine patients with lateral foot or plantar midfoot pain for tenderness along the plantar course of the peroneus longus tendon. It appears to be a structure that is often injured. The first step in diagnosis of a distally injured peroneus longus tendon is suspicion of the injury. After determining that there is a likely peroneus longus injury, direct your attention to the lateral ankle. Tenderness of the lateral ligaments is a confirmatory sign of inversion injury. Often the inversion injury does not appear major and tenderness is only seen at the anterior talofibular ligament. An MRI can be of assistance and prevent a mistaken diagnosis of “cuboid syndrome”.
Longitudinal tears of the peroneus longus tendon at or proximal to the cuboid tunnel can often be treated with immobilization. If these tears fail to heal, excision of nonviable tissue and suturing may be performed. An enlarged peroneal tubercle should also be removed. Look to see if a peroneus quartus inserts into the tubercle. Complete peroneus longus tendon tears occur most often at the cuboid tunnel, sometimes in conjunction with an os peroneum. The os peroneum can retract proximal to the calcaneocuboid joint when the distal tendon is torn. If an end-to-end repair is not possible, one may either perform a tenodesis to the peroneus brevis or alternatively attach the longus to the cuboid.
Physical examination of the plantar aspect of the foot must be meticulous. Often an injury to the peroneus longus tendon in this location is missed. Avulsion from the tendon’s insertion into the base of the first metatarsal or medial cuneiform is possible. Usually surgical repair is not necessary for tears of the peroneus longus tendon in this region. Diagnosis followed by immobilization and adequate time for healing is vital. If pain and swelling persist, consider removing non-viable tissue and perform a tenodesis to the peroneus brevis. (Slater 2007)
Follow the link for more information on injury and rehabilitation of the Peroneal Tendon Complex.
|“... A high level of suspicion combined with careful examination should lead to the proper diagnosis. Treatment failure often follows a failure to make the correct diagnosis. ..."
Flexor Hallucis Longus Tendinopathy
The flexor hallucis longus is a multijoint muscle which plantar flexes the hallux, contributes to resisting pronatory forces and is a weak plantar flexor at the ankle, although in the ballet dancer it is the important force transfer link in attaining the point position. Flexor hallucis longus (FHL) tendinopathy is known to be a frequently encountered injury among ballet dancers. In ballet dancers FHL tendinopathy can be found in association with a symptomatic os trigonum. Scattered reports exist of injuries to this tendon in runners. (Coghlan and Clarke 1993) Olaff, in a study of non-athletes noted that this is likely an underreported injury. (Oloff and Schulhofer 1998)Most authors have found that the majority of the injuries to this tendon to take place proximally, with some tears occurring at the level of the hallucal sesamoid bones.
Our concern here is with tendinopathy within the “zone of confusion”. Most clinicians do not have injuries to this tendon high on their list of suspected causes of plantar and medial foot pain. In addition to the widely described common areas of injury, be certain to examine the plantar midfoot carefully and palpate this tendon. The term flexor hallucis longus dysfunction appears most appropriate and should be included in a differential diagnosis for pain in the medial foot or plantar medial foot. The symptoms may overlap with that of plantar fasciitis, tarsal tunnel syndrome, and insertional posterior tibial tendinopathy. (Schulhofer and Oloff 2002)
Tenography may be an accurate indicator of injury to this tendon, but is no longer widely used. Physical examination, MRI, and diagnostic ultrasound could be useful in the diagnosis of this clinical entity. Physical examination will reveal tenderness along the course of the FHL tendon. Limitation of dorsiflexion of the hallux may be found. Pain may be elicited by dorsiflexion of the hallux or dorsiflexion at the ankle.
FHL tendinopathy has been found in conjunction with plantar fasciitis. (Michelson and Dunn 2005) Upon questioning, the patient will often reveal that they have been performing vigorous dorsiflexion exercises of the toes and hallux in attempting to “stretch” the plantar fascia.
Differential Diagnosis of FHL Tendinopathy
- Symptomatic os trigonum
- Posterior impingement syndrome
- Steida’s process fracture (Shepherd’s fracture)
- Posteriomedial talar osteochondral injury
- Subtalar joint coalition
- Posterior tibial tendinopathy
- Flexor digitorum longus tendinopathy
- Peroneus longus tendinopathy
- Partial tear of the plantar fascia
- Plantar fasciopathy
- Hypertrophy of the FHL muscle and compression within the fibro-osseus tunnel
Conservative treatment is often useful and yields excellent results in the plantar midfoot. Dorsiflexion exercises of the great toe and vigorous over stretching of the Achilles tendon should be discontinued. Short term immobilization may be necessary. Eliminate over cushioned and excessively flexible shoes. Following weaning from a cam walker or pneumatic walker, begin soleus and gastrocnemius stretching and strengthening. Recommend a running shoe that is a good match for the patient’s individual biomechanics.
Follow up exercises after resolution of symptoms should include gentle calf stretching, toe curls to improvement intrinsic muscle function, and wobble board exercises to develop ankle strength, stability, balance and proprioception. An orthotic as described below is often helpful.
The surgical treatment described includes debridement, tenolysis, decompression, and excision of a symptomatic os trigonum. The reported surgical results for proximal injuries have been excellent. (Michelson and Dunn 2005; Hamilton 2008) The patient should be kept non-weightbearing for two to three weeks. Begin gentle hallux range of motion exercises at 7 days. Following the non-weight bearing time period, transition to pneumatic walking boot for two weeks, then wean the patient from the pneumatic walking boot.
Orthotic Therapy for Peroneal Tendinopathy
Orthotic therapy can be helpful for peroneus longus tendinopathy following resolution of the bulk of the symptoms. The major function of the orthotic should be to decrease supinatory moments and forces around the subtalar joint. At its insertion into the base of the first metatarsal and medial cuneiform the peroneus longus becomes a supinator of the foot by virtue of its plantarflexory function at the first ray. In certain foot types however, the peroneus longus can create a pronatory force by its "lifting" effect below the "pulley" of the cuboid groove. Tension will be relieved within the tendon by lessening supinatory moments and diminishing lateral overloading forces. (This can also be helpful for fifth metatarsal, cuboid stress reactions, and peroneus brevis tendinopathy.)
The orthotic planning begins with a proper cast. For polypropylene shell orthotics, an off weightbearing plaster casting technique should be used. The midtarsal joint should be maximally pronated while the subtalar joint is held in neutral. Forefoot supinatus should be eliminated by plantarflexing the first ray by applying a plantar flexion force on the dorsal aspect of the first metatarsal head. (Sometimes mild dorsiflexion of the hallux can assist in creating a mild plantarflexion of the first ray.) An intrinsic forefoot post needs to be used with this casting technique. The Features of an orthotic prescription should include a forefoot valgus extension below the second through fifth metatarsals (approximately 3 degrees), a flat and stable rearfoot post with no rearfoot post motion grindoff ( 0/0 at some labs), a lateral heel skive (Kirby), no beveling of the lateral aspect of the rearfoot post and cast balancing using a vertical or slightly everted cast pouring. Moderate cast fill is usually used, but consider minimal cast fill for better conformation to the foot shape and contours. Direct milled orthotics can be helpful in providing stability. A 3 mm to 5 mm heel lift can also be helpful in reducing the tension in the peroneal tendons.
The rationale for this prescription is first to decrease supinatory moments (in layman's or simplified terms - rotational forces) at the rearfoot (STJ). Secondarily the stability of the rearfoot post combined with the diminished supinatory moments will both decrease tension within the tendon and also prevent a sudden inversion which will create a stretch and stretch response reflex.
We have reviewed several troubling injuries. Diagnosis is the key to successful treatment of injuries. Careful assessment and review of differential diagnoses should lead to the proper diagnosis. Regular critical review of the available literature will keep your knowledge up to date. Successful diagnosis and treatment of your patients is the first step towards overall success.
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