Jan 29, 2015Starting at the Bottom
When the complaint is recurring pain in the heel, bone spurs may be the cause. Treating this condition means looking at the full functional capability of the athlete.
By Casey Smith & Dr. Micheal Clark
Casey Smith, MS, ATC, PES, CES, is Head Athletic Trainer for the NBA’s Dallas Mavericks. Micheal Clark, DPT, MS, PT, CES, PES, is President and Chief Executive Officer at the National Academy of Sports Medicine. They can be reached at: [email protected].
If you’re like most athletic trainers, your rehab cases typically deal with acute-onset injuries that have clearly defined parameters of structural damage, common etiology, and consistent presentation. Even chronic injuries such as stress reactions or tendonopathy usually have a predictable set of signs and symptoms. Rehabilitation protocols are common and available, and a timeframe for return-to-play can be set with relative certainty.
But some cases are less straightforward: the aches and pains come at seemingly random intervals. When our athletes present with chronic conditions that they have always “just dealt with,” how do we assess and treat them? Sometimes the complaint is, “My knee always hurts.” Other times it’s “I have weak ankles,” or “I just always feel tight.”
Often, the athlete gets by with some ice, electrical stimulation, and ibuprofen. But the chronic pain is a cue that there’s an underlying condition, and the way we evaluate and treat these complaints can significantly impact performance and longevity. In our constant effort to prevent injuries, not just react to them, this should be viewed as an important professional challenge.
A good example involves the formation of bone spurs. Some athletes compete successfully and consistently with a mild case of bone spurs, so there is a tendency to treat only the symptoms. And without a straightforward rehab protocol, there is usually not much professional guidance.
However, we must resist the urge to be satisfied with the status quo for athletes with this condition. Instead, we must develop unique rehab protocols that address the chronic pain and its root causes.
WHAT ARE BONE SPURS?
As year-round training and competition have become more and more common, athletes’ bodies need to adapt. We know that the body responds to the stresses placed on it—this principle is the foundation for strength, endurance, and flexibility gains. Muscle hypertrophies follow strenuous loading, connective tissue aligns and lengthens with tension, and the inherent strength of bone is increased by repetitive loading. These are all desired outcomes that follow consistent patterns in a healthy person.
But what about the physiological responses to stresses that are unwanted or not optimal for performance? Tension from structures that attach to bone is often met with increased bone production at the tension site as a protective mechanism, which can lead to the development of a spur. This is beneficial for maintaining the integrity of the attachment, but at some point it becomes detrimental to the function of the affected area. The spurring deviates from what is considered “normal” anatomy and can lead to a host of orthopedic problems.
Bone spurs often occur in the heel. Other common sites in the athletic population are at the distal attachment of the quadriceps tendon, the proximal origin of the long head of the biceps brachii tendon, the adductor tubercle on the distal femur, and the proximal origin of the hamstring tendon.
What underlying factors lead to bone spurs? Let’s use the heel as an example. Tightness of the gastrocnemius-soleus complex and the plantar fascia place longitudinal stress upon the attachments of the connective tissue to the calcaneus. This leads to a bone spur on the plantar aspect of the foot when the plantar fascia is involved, and on the posterior heel when the common tendon of the gastrocnemeus-soleus complex is involved.
Spurring can also occur extra-articularly, with formations at the distal fibula and tibia along the lines of stress created by ligamentous structures. X-rays reveal that spurring in this area may limit ankle motion in eversion and inversion. Intra-articularly, spurs can occur at the talus within the sub-talar joint. They may occur anteriorly from contact with the anterior distal tibia, or posteriorly from contact with the calcaneus.
Surgical intervention is sometimes required, but in many cases when the spurring is largely asymptomatic, the condition is treated with rest and conservative management. Reducing the tension in the connective tissue and musculo-tendinous unit is an important step in managing bone spurs, since it can prevent recurring pain and inhibit the further development of spurring.
A DEEPER LOOK
The anatomy of the ankle is complex, with multiple ligaments supporting bony structures, muscles attaching to and crossing the joints, and the arthrokinematics of the bony structures functioning in all three planes of motion. In preventative therapy, we must remember the full dynamic functional components of the musculature, not merely their function in moving the insertion toward the origin in a concentric fashion.
For example, we must remain aware that the gastrocnemius and soleus perform not only force production in plantar flexion of the foot and ankle, as in a jumping motion, but also take on an even greater role in force reduction, for instance when landing from a jump. Likewise, the posterior tibialis not only performs force production in plantar flexion and inversion of the foot and ankle, but also has significant responsibility for force reduction and stabilization of the mid foot during the stance portion of gait.
These are only two examples of how we must consider the function of the musculature as we look to control the mechanics of the foot and ankle. The key is to be aware of all the functional mechanics of the muscles and joints before we formulate rehabilitation and strengthening programs. A program will only be successful if we can reduce the abnormal forces that are causing the bone spurs.
How do we find those abnormal forces? In ankle function, there are two potential problems to look for. One is increased longitudinal tension at the tendinous or ligamentous attachment—a tight Achilles complex causing a posterior calcaneal spur. The other is altered arthrokinematics that allow increased contact between the surface areas of adjacent bony structures—spurring at the junction of the distal tibia and talus. Controlling these unwanted forces can help limit the formation of spurs.
We recently worked with a professional basketball player who suffered from bone spurs in his heels. A veteran who averages more than 35 minutes a game, his report revealed numerous past bilateral and lateral ankle sprains. He told us he’d “always had weak ankles.”
He described sporadic effusion and pain, not related to trauma and seemingly unrelated to activity level, in both ankles. The right ankle was more symptomatic than the left. He had been told that this pain was most likely due to bone spurs.
Past treatment had consisted of a reduction in physical activity, modality treatment, and the occasional use of NSAIDs. His traumatic lateral ankle sprains had been treated with RICE protocol, restoration of range of motion, strengthening of the musculature around the foot and ankle, and proprioceptive training.
The athlete practices and competes wearing a very rigid tape job, and has worn lace-up ankle braces at times to provide additional support, although he prefers not to. When we began working with him, he was asymptomatic.
We strongly believe in the benefits of proper screening to identify underlying problems, so that was our first step. In our screen, we look for biomechanical inconsistencies, strength deficits, and flexibility concerns.
Our evaluation revealed a bilateral cavus foot (rigid, high arch), normal inversion, limited bilateral eversion, limited bilateral dorsiflexion, and on the right, significant rigidity of the first metatarsal phalangeal joint. Strength was normal throughout, and he did not present with significant ligamentous laxity. X-rays of the ankles revealed multiple sites of spurring at the distal fibula, distal tibia, and anterior portions of the tibia and superior talus.
From there, we looked more closely at a few findings from his initial evaluation. The history of chronic lateral ankle sprains would indicate ligament instability, yet the objective examination revealed stable ligamentous structures. In fact, we even found decreased ligamentous flexibility in certain motions, even though we might guess it would be increased. What could be a predisposing factor?
When the foot is dorsiflexed, the talus moves posteriorly to fill the space in the mortise of the ankle between the distal tibia and fibula. This places the talocrual joint in its most stable position. If the ankle lacks dorsiflexion, it can never get to its most stable position, and may be susceptible to sprains.
The motion restriction at the first metatarsal-phalangeal joint also needed to be considered. Because limited motion at a joint within the kinetic chain causes associated structures to incur a greater amount of stress, we wanted to make any related insufficiencies elsewhere in the kinetic chain part of our treatment plan.
PLAN OF ACTION
With an idea of the problem, we developed two goals for the athlete: to improve motion restriction and to strengthen any muscles inhibiting the full kinetic chain of motion. To address the first goal, we wanted to return the arthrokinematics to as near normal function as possible, so we implemented joint mobilization of the subtalar joint, calcaneus, distal tibia, and fibula, and restriction of the right-side first metatarsal-phalangeal joint.
Anytime there are limitations in range of motion, the antagonistic muscle will be functionally weak. This can be explained by the length-tension relationship that exists in all muscles. Muscles function optimally from a certain length. Therefore, if the length of one muscle is compromised by another muscle (making it either too short or too long), then strength, ROM, neuromuscular control, and power will suffer.
For example, if an athlete lacks sagittal plane dorsiflexion, he or she will need compensatory motion in the frontal (eversion) and transverse (external rotation) planes during landing and running. Repetitive compensation in these planes leads to excessive pronation (eversion, external rotation, dorsiflexion). Repetitive pronation alters the length-tension relationship and changes joint arthrokinematics—the medial malleolus and distal tibia are forced into compressive contact with the medial talus.
This compensation would functionally lengthen the posterior tibialis, anterior tibialis, and medial gastrocnemius. Therefore, these muscles have to be “re-trained” to eccentrically control pronation (eversion, external rotation, and dorsiflexion) and isometrically control the talonavicular joint and talotibial joint to prevent abnormal joint arthrokinematics. The soleus is then forced to work too hard. This adaptively shortens the soleus, and a muscle that is shortened will also lack functional force production, force reduction, and stabilization. Therefore, the soleus needs to be re-trained in the proper ROM.
Lack of ankle dorsiflexion causes the tibia to externally rotate and the femur to adduct and internally rotate. This leads to compensatory lengthening of the gluteus maximus and medius. Therefore, these muscles have to be re-trained to isometrically stabilize the sacroiliac and hip joints, as well as to eccentrically decelerate and control the femur during loading.
To meet our second goal, we assessed the structures connected via the kinetic chain. Knee mechanics and general leg strength were within normal limits. Examination at the lumbo-pelvic-hip complex revealed a decrease in internal rotation at the left hip and similar talocrual restrictions right to left.
Traditional Treatment: After acute incidents, we implemented regular use of ice every 90 to 120 minutes around the clock in an acute setting, and five to six times daily in a sub-acute setting. We did this via ice packs or a cold plunge after activity.
We continued the daily taping for practices and games. Attention was paid to reducing the amount of tape that crossed the dorsum of the foot over the talocrual joint. As ascertained by the decreased range of motion, further restrictions at this area would continue to limit ROM.
To accommodate the athlete’s preference, there was minimal use of electrical stimulation or NSAIDs. He also did not want to wear an ankle brace, so we did not ask him to.
Integrated Manual Therapy: During the next phase, primary attention was paid to motion restrictions at the following joints and associated mobilizations:
• Right foot first metatarsal-phalangeal joint: passive mobilization increasing amplitude as functional range improved.
• Bilateral subtalar: mobilizations supine and standing. This was particularly important prior to taping to establish optimal available range of motion.
• Left tibio-femoral joint: passive internal rotation of the left tibia.
• Left hip internal: rotation mobilization with lateral distraction via traction belt with concurrent passive internal rotation.
Along with the motion restrictions, we started manual soft-tissue release of the following structures (distal to proximal):
• Bilateral plantar fascia • Bilateral peroneal complex, L>R • Bilateral lateral gastrocnemius • Left tensor fascia latae • Left distal biceps femoris • Bilateral gluteus medius • Bilateral piriformis, L>R • Psoas, bilateral, L>R
Daily neuromuscular stretching of the following (all bilateral) was another important step:
• Gastrocnemius • IT band, L>R • Hamstrings • Gluteus medius • Piriformis
Corrective Exercise: As mentioned above, we wanted to work on inhibiting motion in certain areas and lengthening muscles in others. We implemented daily self myofascial release (bilaterally) pre and post activity in the following areas:
• Peroneals • Lateral gastrocnemius • IT band • Gluteus medius • Piriformis
Static stretching was performed after activity for optimal lengthening to the:
• Bilateral gastrocnemius • Bilateral soleus • Left biceps femoris • Left piriformis
For activation, we started isolated muscle strengthening for these structures:
Bilateral Poster Tibialis
• Thera-Band plantar flexion combined with inversion and great toe flexion emphasizing eccentric control and endurance, performed in the supine position.
• Single-leg balance with foot control. Maintain neutral subtalar position and actively fire deep posterior musculature of FHL, FDL, and posterior tibialis by firing the toes into the floor or a balance pad. Difficulty is increased via typical mechanisms such as unstable surfaces, upper-extremity motion, and lack of visual input. Should be completed to fatigue.
• Use of ankle isolator or similar apparatus for specific posterior tibialis strengthening.
Bilateral Medial Gastrocnemius
• Double- to single-leg calf raise with internal rotation. Concentrically raise with both feet, slowly lower eccentric over five-second count with only one leg. Take care to fire through the great toe and not drift laterally over the four lateral toes.
• Daily tubing walking—increase resistance with multiple bands if necessary. Emphasize upper-body control and force production from heels without external rotation of the lower extremity. Complete to fatigue.
• Bridging exercises initially. Progress to integrated gluteus maximus exercises in the next section.
When exercises are designed to emphasize endurance, they should be performed to fatigue or loss of eccentric control. The demands of sport require certain muscles to fire thousands of times throughout a given competition or practice. This type of endurance is not gained with simple sets and reps.
The final challenge is to take as many of the isolated activities listed above as possible and combine them into functional activities. Control of the torso and upper body during functional activity is based on the lower extremities, and in particular the foot and ankle, providing a stable platform or base for these movements. Here are some of the exercises we used:
• Progress ball bridging to weighted Russian twist exercise on ball. Maintain hips level, knees and ankles at 90 degrees, and maintain foot contact.
• Lunge with rotation. Emphasize foot control and force through great toe.
• Quarter- to half-squats with the foot neutral and proper alignment of the knee in relation to the foot and ankle. Combined motion as it occurs in the loading phase of squatting (such as prior to a jump) should have the center of the patella moving in the frontal plane over the center of the foot, which is approximately the second toe.
How did the athlete respond? His joint motion improved in every area (see Before & After). He also progressed well with no insidious onset problems, which had been common for him in the past, and no flare-ups in non-contact situations. While he has had a few exacerbations due to landing on opponents’ feet, each case was resolved functionally within 24-36 hours, with residual soreness lasting up to 7 days. In addition, a long-term issue with left side IT band irritation is no longer present.