Vol. 25 • Issue 16 • Page 12
Sports Medicine Focus
Tibialis posterior tendon dysfunction is a commonly misdiagnosed ailment characterized by pain along the medial arch.1,2 Pain associated with this condition causes an array of compensatory movements, which in turn can provoke symptoms from neighboring structures.This spreading of pain and compensatory movements can result in actual structural deformity in the foot. What starts as medial foot pain can lead to a “domino effect” of progressive dysfunction.
Diagnosis of tibialis posterior dysfunction (TPD) is for the most part made clinically through history and physical examination. Radiographs can be beneficial, however, for ruling out other conditions that could otherwise present as medial ankle pain.2
Patients with TPD often clinically present with a diffuse ache by the medial malleolus and instep or arch.2 Subjective complaints are usually without traumatic etiology. The pain is often described as mild to moderate in severity, intermittent in nature, and often worse after prolonged walking or standing.
Pain is most often near the muscle’s distal insertion at the navicular and plantar aspect of the cuboid, cuneiforms, and medial metatarsal bones. Localized edema and tenderness to palpation may present along the course of the tendon.
TPD is commonly falsely attributed to ankle sprains (such as deltoid sprain) or arthritis, given the subjective vague symptomology along the medial foot. Other flat-foot (pes planus) or pronated foot-type conditions can be associated or attributed to TPD. These include diabetes mellitus, neuropathic foot, hypertension, steroid injections around the tendon, arthropathies, fractures, and leprosy.1,2
Due to the tibialis posterior’s role as a dynamic foot and ankle stabilizer, patients often note increased pain while walking outdoors or over uneven terrain. Contraction of the tibialis posterior muscle causes the foot to plantar-flex and invert (down and in). This contraction also elevates the medial arch of the foot and locks the mid-tarsal bones to make for a more firm platform for push-off during gait.2,3
The tibialis posterior thus helps tremendously with gait efficiency by holding the foot in the most optimal position to allow the calf muscles to push weight off the foot.
Specifically during the gait cycle, pain tends to be most pronounced during the stance phase. During this phase, the most pronounced gait abnormalities occur just prior to heel-off through toe-off in patients with TPD.4 This makes sense biomechanically, given the tibialis posterior’s function to stabilize the mid-foot during toe-off.
Along with gait disturbances, impaired balance can be a complaint due to limited dynamic stabilization. Single-leg stance activities requiring lifting of the heel (heel raises) are often difficult and antalgic. Without proper function from this muscle, compensation inevitably ensues.
Progressive Wear and Tear
While TPD may initially start as in inflammatory process (tendinitis), the dysfunction more closely resembles the pathology of tendon degeneration (tendinosis).2,5 With this process, the tendon becomes more fibrous due to repeated microtrauma and overuse.
It’s theorized that the mechanical demands of the tibialis posterior are much greater on a flat foot compared to that of a more normal foot. This could lead to a process of progressive fibrotic wear.
Studies have demonstrated that the wear could in part be due to lack of adequate blood supply to the tendon.5 Review of blood supply (vascularization) to the tibialis tendon reveals certain areas have reduced blood supply.
This zone of reduced blood supply (hypovascularity) was found to be just posterior and distal to the medial malleolus. This area correlates not only with the site of symptoms but also with the site of most pronounced tendon degeneration.
This manifestation makes one wonder “what comes first?” Is it the mechanical demand placed on the tibialis posterior with a flat foot that causes this vascular reduction, or does the tendon simply have a poor blood supply in this area, and a flat foot exacerbates the degenerative process? Further studies should reveal whether TPD causes the blood reduction or whether TPD speeds up the degeneration of a tendon that’s already hypovascularized.
With a compromised platform for push-off, neighboring structures in the foot can become affected. The gait pattern typical of a flat, over-pronated foot position leads to faulty biomechanical movements, which in turn may lead to compensation of the first ray. This pronated foot is a less-stable platform for stance phase through push-off.
As a result, the first ray has more force put on it during the late stance phase and early push-off. This sets up a valgus-type moment on the first ray, which may result in bunions (hallux valgus).
If this pattern of walking is chronic, a toe wedge may be helpful if placed between the first ray and neighboring toe. This restores more ideal anatomical alignment of the first ray and allows the flexor muscles of the first ray to operate more optimally.
Retraining the abductors of the first ray (abductor hallucis) to co-contract with the first ray flexors and extensors may be also be necessary. This will pull the toe out away from the valgus position while simultaneously using the toe in a functional movement pattern (curl toe while pulling toe out). This helps with neuromuscular re-education of the first ray musculature that’s otherwise not allowed to contract ideally in the valgus position.
Stopping the Cascade
Compensation during gait and movements with TPD can progress other foot conditions.2 These altered and compensated movements can directly cause other foot pathologies or aggravate the symptoms of existing conditions. These sequelae-type conditions may include metatarsalgia, hallux rigidus, and sinus tarsi syndrome.
Other objective findings may include a tight or hypomobile calf complex. Careful attention should be paid to stretching the calf muscles without the mid-foot and medial arch falling into a collapsed or pronated position. This may result in pain and inadequate stretching of the calf group.
What can be done to stop this domino cascade of progressive dysfunction? As previously mentioned, gait training, proprioceptive exercises, proper stretching of tight musculature, and neuromuscular re-education of inadequately recruited muscles should be a staple of treatment.
However, much emphasis should be paid to the restoration of foot alignment. This postural correction can come by way of therapist instruction on proper footwear, postural correction exercises, and orthotic fabrication. Studies have shown positive results when orthotics are used to address TPD.
Studies have demonstrated excellent improvements in pain, patient satisfaction, ambulated distance, and function with orthotic use in up to 70% of subjects.6 Furthermore, the wear time for orthotics was just about 12 hours, indicating that it may not be necessary to wear orthotics all the time for all weight-bearing activities.
Although tibialis posterior dysfunction is commonly misdiagnosed, recognizing the condition can help reverse this clinical trend. Greater awareness of TPD has the potential to elicit great results from the rehabilitation community. Therapists have all the diagnostic and interventional skills necessary to effectively treat this condition, and stop the unfortunate trend of progressive dysfunction.
References are available at www.advanceweb.com/pt. Click References under the Toolbox tab.
Ben Wiggin is practice manager of Back Bay Rehabilitation, Tamworth, N.H. Contact: email@example.com.