By Lisa M. Schoene, DPM, ATC, FACFAS
Plantar fasciitis is probably the most common condition that the podiatric physician treats. We all have a myriad of treatment regimens and protocols that ultimately get our patients back on their feet.
Usually, we suggest stretching of the gastrocnemius and soleus muscles very matter of factly. We know that these two muscles distally form the Achilles tendon and that tendon expands around the posterior aspect of the calcaneus to join into the plantar fascia. The plantar fascia or plantar aponeurosis is a thick, fibrous band made of collagen tissues that have a tensile strength of 7,000 pounds per square inch within the central portion.
The fascia splits into three bands: the medial, central and lateral. The medial portion is thinner, originates from the flexor retinaculum and the medial calcaneal tubercle, and blends together with the central portion. The central portion, which is the thickest portion, is triangular in shape as it fans outward and into its distal deep and superficial layers. The deep layer attaches into the flexor tendons of each toe and helps to maintain the fat pads and plantar plates. The superficial layer merges with the transverse metatarsal ligaments. The lateral band originates from the smaller lateral tubercle, covering the abductor digiti minimi muscle and then inserting into the proximal and plantar surface of the fifth metatarsal. Under ultrasound inspection, the medial and central bands normally measure on average 2.5 to 2.7 mm thick from dorsal to plantar, and the lateral band should measure about 1.7 to 1.9 mm thick.
Due to the proximal attachments into the Achilles tendon, it would make sense that calf stretching both with the knee straight and with the knee bent would be an important part of the treatment protocol. Stretching will lessen the strain or pull into slips of the plantar fascia band from proximal to distal.
Looking at the anatomy, we know that a tight gastrocnemius and/or soleus muscle will result in a loss of dorsiflexion range of motion at the ankle joint. Tightness that predominates with the knee straight would suggest the gastrocnemius is tight whereas tightness with the knee bent would indicate that the soleus is the culprit. Either way, we typically define this as equinus.
There are many etiologies of equinus. These include spastic equinus, like one would see with cerebral palsy or high muscle tone issues, congenitally short musculature, prolonged casting, limb length discrepancies, a plantarflexed forefoot deformity, excessive use of high heels, lack of stretching, and/or general muscle weakness. Ultimately, partial or fully compensated equinus will produce some untoward effects within the foot and/or up the kinetic chain. When compensation occurs, it has to affect another area of the body.
The definition of “compensation” is a good thing to review since we treat many of the maladies it causes. The definition of compensation is an abnormal change of structure, position or function of one body part or joint in the attempt to neutralize the effects of improper deviations, positions, functions of another body part or joint. Given the profound nature of compensation, the true work of the thoughtful podiatrist can therefore change everything from head to toe. What happens “to,” “from” or “within” the foot will ultimately affect something else in the body. What will happen? Will that compensation go distally or proximally?
While discussing compensation patterns, there are other factors that may impede or enhance the situation. These factors are: ligamentous laxity, which allows joints to have much more mobility than they should; improper shoe gear such as unsupportive shoes; and even suprastructure issues, such as genu valgum, malicious malalignment syndrome, poor pelvic excursion, structural tibial and/or femoral rotational issues. The compensations along with any of these issues will unfortunately occur up and down the kinetic chain for all to see.
Compensations can and will occur at these midtarsal joint, the subtalar joint and the first ray.
Midtarsal joint. True full compensation of a decreased ankle joint range of motion (ROM) will cause potential collapse of the more obliquely oriented joint axis that moves the midtarsal joint. This would cause talar plantarflexion, forefoot abduction, the “too many toes sign” and possibly severe hallux abducto valgus, hammer digit syndrome, and even the rocker bottom type foot. Tendon pathology is also common. This is not a pretty foot and we have all seen it coming from a mile away. Compensation here produces prolonged abnormal pronation.
Subtalar joint. When partial or full compensation occurs in the subtalar joint, it causes the rearfoot/calcaneus to evert past the norm, thus straining the alignment, length and motor function of the intrinsic and extrinsic foot musculature. When this occurs, hammertoes or other forefoot deformities can develop in the foot and tendinous strains may occur such as posterior tibial tendon dysfunction. Compensation here also produces prolonged abnormal pronation.
First ray. Due to the obliquity of the axis of the first ray, partial or full compensation here will cause the first ray to dorsiflex and invert. If this occurs, first metatarsophalangeal joint (MPJ) function becomes limited, producing functional and/or potentially structural hallux limitus/rigidus. This chronically elevated first ray can be devastating as it impedes the normal lever needed for forward progression of gait. Couple this with the areas of compensation I mentioned above and there may be a poor outcome. Alone, this compensated joint can produce its own set of complications up the chain, even into the temporomandibular joint. Quite often, we may hear complaints of neck pain or headache after dispensing orthotics. This is not a coincidence but rather the work of changing the compensation patterns that the body is so used to. Changing them makes the fascia and musculature pull in a way they are not used to, resulting in strains.
Equinus and its path of destruction can also affect the knee joint because when the talus adducts and plantarflexes, internal rotation occurs at the tibia. This can contribute to patellofemoral syndrome, chondromalacia and iliotibial band friction syndrome. Over time, internal rotation at the tibia may even generate enough chronic rotational forces to damage the menisci. In general, longstanding gastroc equinus may directly cause genu recurvatum, which can show up in early adolescence.
With continued internal rotation of the tibia comes internal femoral rotation. When this occurs, there is rotational pull through the hamstrings, which may produce chronic strain distally or proximally. Additionally, there may be strain at the sacroiliac joints and stress and strain to the external hip rotators, namely the piriformis. When overzealous traction occurs here, irritation to the sciatic nerve may occur, producing radicular pains into the buttocks and even the leg. Add a leg length discrepancy or other scenarios, and it turns out to be a real pain in the butt.
If all of these compensations occur unilaterally, single foot abnormal pronation may induce unleveling of the limbs, possibly causing a leg length discrepancy and abnormal shear within numerous muscles of the lower extremity. Additionally, with abnormal pronation, the proper motor patterning of the gluteal muscles will be affected. This subsequently affects normal gait, limiting proper extension and may allow for weakness of hip abduction, which we call the Trendelenburg gait.
Continuing up the kinetic chain, the lower back as well as the thoracolumbar areas may suffer as well due to the abnormal rotational compensations. The excessive internal rotation could produce shearing of the lumbar discs, causing potential bulging or degenerative arthritic changes. Accordingly, clinicians may commonly note a disc bulge incidentally. Often when it ruptures, the patient was not doing any excessive movements and this probably would not have occurred if there were not chronic low-grade rotational compensations occurring at these areas. Lower back postural fatigue is common and we can often remedy this when we look toward the foot for the answer.
When there are frontal, transverse or sagittal plane compensations, rotation of the pelvis will be affected so any or all of the musculature attaching to the pubis and ilium are susceptible to abnormal strain. The affected musculature may include the abdominal musculature, psoas muscles, tensor fascia lata and the hip adductors. Impaired recruitment here may lead to chronic weakness and the gait changes I mentioned above.
Moving proximally, the quadratus lumborum and erector spinae muscles attach to the ribs, illium and lumbar vertebrae. The muscular and aponeurotic diaphragm forms the floor of the thorax and the roof of the abdomen. The diaphragm originates from the superior lumbar vertebrae, its ligaments and the lower ribs. Extensive arteries, the phrenic and intercostal nerves, and lymphatic vessels supply and pass through the diaphragm. When mechanical compensation patterns persist throughout the trunk, due to what is occurring in and around the foot and ankle, could we imagine that vessel, nerve and lymphatic flow are altered or affected?
This list sounds daunting and it is unlikely that all of the scenarios will occur simultaneously. However, we must realize what happens to a foot can affect the whole kinetic chain, not just for treatment of plantar fasciitis, but for a whole host of conditions and diagnoses that we evaluate and treat. Every change we make to the foot — whether it is with a shoe, pad, surgical procedure or orthotic device — will ultimately affect other joints, tissues, tendons and fascia. We know that performing a flatfoot procedure without lengthening the Achilles is unthinkable. Understanding and reviewing the anatomical connections that every muscle, joint and ligament share will make every physician realize the importance and the magnitude of stretching the gastroc and soleus for all of the biomechanical conditions we treat.
We have always been the biomechanical experts in the field of foot pathology but that accomplishment is slowly fading away as we continue down the path of medical parity. We cannot eliminate the essence of who we have been as podiatric physicians. As our surgical prowess continues to grow, we cannot forget the biomechanical teachings and workings of the foot joints as every mechanically-based surgical procedure will fail without this knowledge.
Let us get back to our roots of what distinguishes us from the other practitioners who treat foot conditions. The combination of evolving surgical genius with the reinvigorated research, use and love of biomechanics can catapult us out of the park as the experts in the foot and ankle. This will solidify our status and make us very valuable specialists in the ever changing healthcare marketplace.
Dr. Schoene is a triple board certified sports medicine podiatrist and a certified athletic trainer. She is a Fellow of the American Academy of Podiatric Sports Medicine and the American College of Foot and Ankle Surgeons.
For further reading, see “Plantar Fasciitis: How To Maximize Outcomes With Conservative Therapy” in the May 2006 issue of Podiatry Today.
By Stephen Pribut, DPM, FACFAS
Stretching may be the most frequently recommended treatment for plantar fasciitis (fasciopathy).1,2 Several articles highly recommend calf stretching and specific plantar fascial stretching.3 But is stretching right for every case of plantar fasciitis? Is it always correct to recommend stretching? Without any reservations but with some nuance, I will say no.
Is more stretching the only conservative therapy we have to offer the patient who visits after six months of dutiful stretching? The wisdom of the Internet would lead us to rolling with a golf ball, icing, more stretching and over-the-counter inserts for plantar fasciitis. We can do better.
Some studies using stretching as sole therapy have focused on patients who have had plantar heel pain for less than six weeks, limited to one foot and have had no prior therapy. A recent study compared plantar-fascia specific stretching with shockwave therapy for the initial treatment of unilateral plantar fasciopathy for an average of four weeks.4 The authors found that “stretching” the plantar fascia was superior to shockwave at the four-month mark but had no superiority at 15 months. The study excluded nearly a third of the patients selected as they refused to sign the consent form for the study. In addition, 10 to 15 percent of the study patients became lost to follow-up for the data acquired at 15 months.
If stretching has had minimal impact, we need to evaluate our therapy and change it. The literature of chronic plantar fasciitis usually looks to solutions that involve other modalities besides stretching.
The plantar fascia is primarily made up of linearly oriented fibers mainly comprised of collagen. A recent study demonstrated that the fibers run primarily proximal to distal with layers of fibers oriented vertically, transversely and obliquely.5 This multilayered structure is characteristic of a tissue that has much of the nature of a “fascia” and not an aponeurosis. The strain resistance characteristics of the plantar fascia are much stronger than much of other fascia and the plantar fascia’s strain resistance is similar to the iliotibial band.6
The plantar fascia, in part, functions as a windlass mechanism and much biomechanical theory posits that the foot needs to act as a mobile adaptor at contact and as a rigid lever at the propulsive phase of gait.7 The fascia elongates as the foot proceeds through midstance and more strain develops as the heel leaves the ground and the digits dorsiflex.8 The plantar fascia and plantar muscles absorb the loading forces as elastic strain energy early in gait and return it later as passive elastic recoil.7,9 Importantly, the plantar fascia and plantar muscles contribute to the function of the foot as a rigid lever. Stiffness is an important and needed feature of the longitudinal arch late in gait. The plantar fascia and the windlass mechanism are the major contributors to this stiffness.
Researchers have long hypothesized that the plantar intrinsic foot muscles contribute to resisting loading forces and act to increase the height of the longitudinal arch. Only recently have researchers been able to test and demonstrate that activation of three plantar intrinsic muscles (the abductor hallucis, flexor digitorum brevis and quadratus plantae) had this effect.10 Electrical stimulation of the plantar muscles acts to counter the deforming force of an external load and resist the lengthening of the “arch” and lowering that would otherwise occur. Earlier models often emphasized the function of the plantar fascia but added a “viscous damper” to the model and worked on the premise of the plantar intrinsic muscles acting parallel to the plantar fascia.11
Anatomical and histological studies of the plantar fascia show that Pacinian and Ruffini corpuscles are present in the plantar fascia.5 This indicates that the plantar fascia may play a role in foot proprioception and perhaps in triggering muscle function and coordination. Through this mechanism, the plantar fascia may contribute to overall balance and posture.
The fibers that stretch in the posterior musculotendinous system are predominantly in the muscle. Tendon does not stretch well or easily although its compliance is alterable by some types of stretching. Likewise, the plantar fascia is not easily stretchable and I believe that efforts to stretch the plantar fascia may end up also acting on the intrinsic muscles and tendons. There is indirect evidence that this occurs clinically and I will discuss this further below.
While studies have attempted to determine the existence of an anatomical connection between the Achilles tendon and the plantar fascia, the mechanical linkage is not in question.12 They both have in common a connection to the calcaneus with actions that are in opposition. An Achilles tendon and calf muscle that are tight are going to place added strain on the plantar fascia.
Alfredson, a strong proponent of eccentric stretching and a major theorist of Achilles tendon injury, strongly warns against eccentric stretching for insertional Achilles tendinopathy.13 Alfredson considers the insertion point to be a weakened and vulnerable area when it is injured. I would suggest that the enthesopathy of plantar heel pain is another area where caution is advisable.
A 2005 study of flexor hallucis longus tendinopathy found that more than half of the study patients had prior therapy for plantar fasciopathy.14 The authors noted a close correlation of flexor hallucis longus tendinopathy with other areas of symptoms, particularly the plantar fascia. The conservative treatment group did not do well. A mainstay of their previous therapy was likely stretching of both the calf muscles and the plantar fascia. I conjecture that manual dorsiflexion of the toes, including the hallux, may have triggered the flexor hallucis longus tendinopathy.
I see this often in clinical practice. If you look for flexor hallucis longus tendinopathy in patients presenting with plantar fasciopathy, you will often find it in patients who have spent considerable efforts in “stretching” their plantar fascia by dorsiflexion of the toes and, in particular, the hallux.
Stretching is not a warm-up. Stretching should follow exercise or after patients have warmed up. The best warm-up is to perform slower and gentler movements and exercise than you will be undertaking in your sport.
Static stretching may inhibit performance. Studies demonstrate a weakness and performance decrease following static stretching of the ankle plantarflexors.15,16 The decrease in performance may be due to neural inhibition rather than an alteration of muscle and tendon mechanical properties. This is one reason why pre-exercise static stretching has gone out of vogue.
Is stretching always appropriate? Stretching is a reasonable approach to an early, mild to moderately painful presentation of plantar fasciitis. It is not appropriate as the sole treatment for chronic plantar fasciitis.
Stretching is not as simple an undertaking as it seems. There is static and dynamic (formerly ballistic) stretching, and there is active and passive stretching. In static stretching, the body segments are not moving while in dynamic stretching, there is motion. In active stretching, the muscles are contracting. In passive stretching, the muscle contractions are minimized.
Over the years, different types of stretching have gone in and out of fashion. Coaches of the 1970s recommended ballistic, active and dynamic stretching. Physicians originally condemned ballistic stretching only for that stretching style to come back again in a more sophisticated manner. Different stretches have uses for different problems at different stages of training. A combination of stretch types is likely to be more useful than only one specific stretch type.
The first person to suggest that over-stretching could lead to problems was Schuster. While puzzling over survey data indicating that more stretching led to more injury, Schuster suggested that over-stretching might lead to a higher incidence of injury.17 More recently, D’Amico has suggested that initial treatment of plantar fasciitis should stop all stretching.18 D’Amico also suggested using a shoe with a rigid shank and a heel lift.
Recommend quadratus plantae and intrinsic muscle strengthening in most cases of plantar fasciopathy. These muscles function parallel with the plantar fascia along the plantar surface of the foot. There is enough evidence that intrinsic muscle strengthening should become the major recommended intervention for plantar fasciitis. There are no clinical studies that I am aware of but they would be easy to do. Strengthening the plantar muscles should reduce the strain along the plantar fascia.
There are several ways to perform intrinsic muscle strengthening exercises. I prefer performing the exercises in a manner similar to the way patients use the muscles while walking or running. I recommend rhythmic contractions without holding the contraction for long. Patients tolerate this exercise well and it is a great adjunct to other recommendations.
Gentle stretching of the posterior muscle groups can be helpful. Patients should discontinue stretching that is too vigorous or causes pain during or after the stretch.
Advise patients to avoid open back shoes and flat shoes. Use a heel lift. Beware of those running shoes that used to have a 12 mm heel drop and now have an 8 mm drop. These all increase strain at the Achilles tendon which, translated through the calcaneus, causes increased strain in the plantar fascia.12
Avoid over-stretching of the calf and plantar fascia. Consider a heel lift to lessen the pull on the calcaneus by the calf muscles.
Do not make an orthotic with a low heel cup and “wipe out” the flexible plantarflexed first ray in your casting. Check the latest evidence-based literature on orthotics and consider a valgus post if appropriate.
Read the current literature. The old literature was wrong on many things. The current literature represents an approach that is subject to revision. Tomorrow’s literature will offer different solutions and promise better results.
Treatment often requires a nuanced approach. While we have a pro and a con side presented in these Point-Counterpoint articles, I really hope we have inspired you to think about the solutions you present and the study design in the articles you read. n
Dr. Pribut is a Clinical Assistant Professor of Surgery at the George Washington University School of Medicine and Health Sciences in Washington, DC. He is a Fellow of the American College of Foot and Ankle Surgeons.
1. Pribut S. Current approaches to the management of plantar heel pain syndrome, including the role of injectable corticosteroids. J Amer Podiatr Med Assoc. 2007; 97(1):68-74.
2. DiGiovanni BF, Moore AM, Zlotnicki JP, Pinney SJ. Preferred management of recalcitrant plantar fasciitis among orthopaedic foot and ankle surgeons. Foot Ankle Int. 2012; 33(6):507-12.
3. DiGiovanni B, Nawoczenski DA, Malay DP, et al. Plantar fascia-specific stretching exercise improves outcomes in patients with chronic plantar fasciitis. A prospective clinical trial with two-year follow-up. J Bone Joint Surg Am. 2006; 88(6):1775-1781.
4. Rompe JD, Cacchio A, Weil L Jr., et al. Plantar fascia-specific stretching versus radial shock-wave therapy as initial treatment of plantar fasciopathy. J Bone Joint Surg Am. 2010; 92(15):2514-22.
5. Stecco C, Corradin M, Macchi V, et al. Plantar fascia anatomy and its relationship with Achilles tendon and paratenon. J Anat. 2013; 223(6):665-76.
6. Chaudhry H, Schleip R, Ji Z, et al. Three-dimensional mathematical model for deformation of human fasciae in manual therapy. J Am Osteopath Assoc. 2008; 108(8):379-90.
7. Wright DG, Rennels DC. A study of the elastic properties of plantar fascia. J Bone Joint Surg Am. 1964; 46:482-92.
8. Hicks JH. The mechanics of the foot. II. The plantar aponeurosis and the arch. J Anat. 1954; 88(1):25-30.
9. Ker RF, Bennett MB, Bibby SR, et al. The spring in the arch of the human foot. Nature. 1987; 325(7000):147-9.
10. Kelly LA, Cresswell AG, Racinais S, et al. Intrinsic foot muscles have the capacity to control deformation of the longitudinal arch. J R Soc Interface. 2014; 11(93):20131188.
11. Kim W, Voloshin AS. Role of plantar fascia in the load bearing capacity of the human foot. J Biomech. 1995; 28(9):1025-33.
12. Carlson RE, Fleming LL, Hutton WC. The biomechanical relationship between the tendoachilles, plantar fascia and metatarsophalangeal joint dorsiflexion angle. Foot Ankle Int. 2000; 21(1):18-25.
13. Alfredson H, Ohberg L, Zeisig E, Lorentzon R. Treatment of midportion Achilles tendinosis: similar clinical results with US and CD-guided surgery outside the tendon and sclerosing polidocanol injections. Knee Surg Sports Traumatol Arthrosc. 2007; 15(12):1504-9.
14. Michelson J, Dunn L. Tenosynovitis of the flexor hallucis longus: a clinical study of the spectrum of presentation and treatment. Foot Ankle Int. 2005; 26(4):291-303.
15. Weir DE, Tingley J, Elder GC. Acute passive stretching alters the mechanical properties of human plantar flexors and the optimal angle for maximal voluntary contraction. Eur J Appl Physiol. 2005; 93(5-6):614-23.
16. Fowles J, Sale D, MacDougall J. Reduced strength after passive stretch of the human plantarflexors. J Appl Physiol. 2000; 89(3):1179-1188.
17. Schuster R. Comments on running injuries and stretching. Personal communication.
18. D’Amico J. Plantar Fasciitis: The Seinfeld Solution. Richard O. Schuster Memorial Biomechanics Seminar, New York College of Podiatric Medicine, New York, NY, 2013.