Porter & Schon: Baxter's The Foot and Ankle in Sport, 2nd ed.

Section 2 - Sport Syndromes

Chapter 9 - Nerve disorders and plantar heel pain




Lower-extremity nerve injuries in athletes






Joint pain of neural origin



Peroneal nerve injuries



Posterior tibial nerve injuries



Less common lower-extremity peripheral nerve problems






Further reading



Plantar heel pain



Fat pad insufficiency



Insertional plantar fasciosis



Entrapment of the first branch of the lateral plantar nerve



Tarsal tunnel syndrome



Midsubstance plantar fasciitis







A A. Lower-extremity nerve injuries in athletes

  1. Lee Dellon


It is my honor to write this chapter for the current edition of the book first edited by Donald E. Baxter, MD, and now edited by David Porter, MD, PhD, and Lew C. Schon, MD. Lew Schon, MD, and Don Baxter, MD, wrote correspondingly the first two authoritative chapters on this subject in 1994. [0010] [0020] Much of what they wrote is now among the “classical” knowledge base of foot and ankle surgeons everywhere. Understandably, it is with trepidation that one approaches any changes in “the classics.” Yet, over the past decade, much has been learned related to the pathophysiology, neuroanatomy, and neurodiagnostic testing techniques that can solidify and augment our approach to that base of knowledge related to lower extremity nerve injuries in the athlete.

Language is a critical part of our ability to make a diagnosis that relates appropriately to our treatment options. In that regard, today the word “functional” often is used in contrast to “organic,” and therefore I feel it is better to describe peripheral nerve problems related to muscular activity as “exercise-induced” rather than “functional,” because “functional” might connote a psychogenic origin. During diagnostic testing for such an exercise-induced problem, the examiner may use techniques that “provoke” the symptoms by creating compression of the peripheral nerve through certain maneuvers, such as the Phalen sign, wrist flexion test for carpal tunnel syndrome, or maintaining the elbow flexed to provoke the symptoms of cubital tunnel syndrome. Therefore the young athlete who complains of dorsolateral foot pain radiating from the lower leg early in the training process, whether running or dancing, should have an exercise-induced compartment syndrome included in the differential diagnosis, because the basis of that pain is acute nerve compression. Similarly, a “neuroma” is the pathophysiologic process of entrapment of axonal sprouts regenerating into scar tissue.[3] A painful neuroma should be treated surgically by resection and implantation of the proximal end into muscle, a technique that has withstood the test of time for the past 20 years for both the upper and lower extremity. [0040] [0050] [0060] [0070] [0080] In contrast, chronic compression of a nerve will create an area of narrowing of the nerve with a swelling resulting from axoplasmic accumulation proximal to that point ( Fig. 9A-1 , A andB). That swelling may appear to be a neuroma but is not a true neuroma. This situation occurs distally in the foot related to the interdigital nerve and the transverse intermetatarsal ligament. The appropriate name for this painful condition should be “interdigital nerve compression” and not “interdigital neuroma.” The history of the origin of this unusual nomenclature has been reviewed recently,[9] and the term “interdigital nerve compression in the (given)-interspace,” although cumbersome, is used in this chapter. Resection of a Morton's neuroma (which is not a true neuroma) results in a true (painful or not) neuroma. Resection is the appropriate surgical treatment for a painful neuroma, and neurolysis is the appropriate surgical treatment for chronic nerve compression.[3] The name we ascribe to a given neuropathologic condition therefore has implications for the surgeon.



Figure 9A-1  Neuronal swelling proximal to the site of chronic compression can cause the appearance of a neuroma, such as in the interdigital nerve to the third webspace (A), or the deep peroneal nerve over the dorsum of the foot (B). In B the extensor hallucis brevis tendon, the source of the compression, has been excised.



The mechanism of injury results in different degrees of nerve injury. Mechanisms may include direct contusion, stretch/traction, laceration, or acute or chronic compression. The pathophysiology, initially subdivided by Sir Herbert Seddon into three groups (neurapraxia, axonotmesis, neurotmesis), then by Sir Sydney Sunderland into five groups (I-V), and finally by Mackinnon and Dellon into six groups,[3]permits diagnosis and prognostication. One could use the knee as an example. The soccer or football player who sustains sufficient force to the medial knee may have a direct contusion to the infrapatellar branch of the saphenous nerve and medial knee pain, which is independent from ligamentous or meniscal structural problems identifiable on a magnetic resonance imaging (MRI). If the infrapatellar branch is simply crushed, recovery of nerve function will be to a normal level, and this will occur within 3 weeks. In contrast, if the force was sufficient to cause disruption of the nerve, bruising, and adherence to the pes anserinus, there will be loss of sensory function and formation of a painful neuroma. If the force of impact is sufficiently great, there may be damage to the meniscus or the collateral ligament, and, in addition to those structural problems, there may be pain resulting from direct damage to the innervation of the knee joint.[10] This leads to knee pain of neural origin in addition to the musculoskeletal problems. There may be sufficient lateral force exerted on the knee to cause complete loss of continuity of the common peroneal nerve in addition to the knee joint or fibular injuries ( Fig. 9A-2 ), resulting in peroneal motor and sensory palsy. Therefore “nerve injury” is an insufficient term to specify the neuropathophysiologic cause of the athlete's pain. Even the term “peroneal nerve palsy” creates ambiguity: Is the correct treatment a period of observation, a neurolysis, or a nerve reconstruction? In this chapter the application of computer-assisted neurosensory testing is included in an attempt to add measurements to the staging of peripheral nerve injury,[11] and therefore to the decision-making process.



Figure 9A-2  During a badminton game, this woman sustained a twisting injury to the right knee and fell, fracturing the fibular head (A). There was an associated complete footdrop. Intraoperatively, at the time of fracture fixation, the common peroneal nerve was completely divided by the stretch/traction injury. The first surgeon reunited the nerve and referred the patient for peripheral nerve reconstruction. The neuroma-in-continuity is identified at the time of reconstruction (B).



Peripheral nerve surgery requires the use of a pneumatic thigh tourniquet, loupe magnification, and bipolar coagulation to properly identify and protect the nerves. In some cases a disposable nerve stimulator is required to identify certain motor functions of the nerve. General anesthesia is preferred. The following is a personal approach to the problems I have encountered in athletes.

Joint Pain of Neural Origin

Knee joint pain can be defined to be of neural origin after any musculoskeletal problems with the integrity of the knee joint have been eliminated from the differential diagnosis or have been treated. A common situation is knee pain in the athlete with an MRI that has been interpreted to be normal. Rest, nonsteroidal anti-inflammatory drugs, and intraarticular steroid injections have not been successful at relieving pain. Arthritis may or may not be present radiographically, and if it is, the patient may have failed to improve with treatment designed to form new cartilage. More than likely the patient will have had one or more knee arthroscopies, at which plica has been removed, cartilage has been debrided, or a synovectomy has been performed, but there is still pain. Could this pain be of neural origin? With the description in 1994 of the innervation of the human knee,[10] it becomes reasonable to consider that the medial or lateral retinacular nerves, or both, have been stretched or torn and have formed a painful neuroma within the joint structures. Indeed, these nerves may have been injured by the arthroscopy itself. ( Figure 9A-3 is an example of a man with bilateral knee pain after years of martial arts, for whom all of the previously mentioned treatments were ineffective and for whom partial knee denervation permitted resumption of daily activities, but not martial arts, without pain. Demonstration of neural origin for the pain is accomplished by (1) local anesthetic block of the suspected nerves, (2) the patient having a decrease in his visual analog scale level of pain by at least 5 points, and (3) observation of improved pain after the block while walking, climbing stairs, and kneeling. If there has been previous knee surgery, a neuroma of a cutaneous nerve, like the infrapatellar branch of the saphenous nerve or the medial cutaneous nerve of the thigh, also must be considered in the examination and the nerve blocks. Figure 9A-4 illustrates the location of these nerves. The first report of partial knee denervation was for patients after total knee arthroplasty,[12] but a subsequent report includes patients with knee pain after sports injuries.[13] A complete description of this subject appeared in the year 2000.[14] The advantage of this approach is that the surgery is performed on an outpatient basis, does not require invasion of the knee joint, and permits immediate ambulation, and rehabilitation can begin when the sutures are removed. Success rates should approach 90% with the previous criteria. Charcot joint does not occur because this is a partial knee joint denervation. The athlete must be counseled that posttraumatic arthritis and synovitis still will occur, but their pain may be significantly lessened.


Figure 9A-3  Partial knee denervation patient 3 months after the left and 6 months after the right knee each had a medial and lateral knee denervation. The 3-cm scars over the medial (right) and the lateral (left) knees are apparent.





Figure 9A-4  Innervation of the human knee joint is illustrated for the lateral (A) and medial (B) views of the knee region. The lateral retinacular nerve originates from the sciatic nerve, crosses deep to the biceps tendon, and innervates the lateral retinacular region. The medial retinacular nerve is the continuation of the femoral nerve branch to the vastus medialis, exits distal and deep to this muscle, and innervates the medial retinacular region.



Lateral ankle joint (sinus tarsi) pain can be of neural origin in the athlete who has had repetitive inversion sprains or a fracture/dislocation of the lateral malleolus. Typically, the inversion sprain is treated with immobilization and anti-inflammatories, and then a progressive regimen of stretching and strengthening is begun. If pain persists and x-rays have not demonstrated a fracture, then a computed axial tomography (CAT) scan with three-dimensional reconstruction is suggested to be sure there are not occult intra-articular fractures or bone fragments within the joint as the source of the pain. Any athlete in any sport can suffer this type of injury. If there is a lax lateral ankle joint, surgery to correct it with ligament reconstruction or tendon transfers (Crisman-Snook, or Watson Jones-types) still may have failed to relieve the pain, although providing good stability (see Fig. 9A-12, C ). If the symptoms extend to the dorsal lateral aspect of the foot, a stretch/traction injury to the peroneal nerve must be considered in the differential diagnosis, and this is considered later in this chapter. If direct pressure into the sinus tarsi reproduces the pain, a local anesthetic block and steroid injection into this region may be given for both diagnosis and for treatment. If the pain persists, then sinus tarsi syndrome is present. Traditional treatment for this disabling condition has been either a “curettage” (debridement) of the sinus tarsi, resection of the lateral shoulder of the talus, or a subtalar fusion. Could this pain be of neural origin? Recently, the innervation of the sinus tarsi has been demonstrated to come from the deep peroneal nerve.[15] The innervation arises most commonly from the most lateral fascicle of the deep peroneal nerve, just proximal to the origin of the innervation of the extensor digitorum brevis in all patients ( Fig. 9A-5). About 25% of patients have a dual innervation of the sinus tarsi from the sural nerve.[15] With this knowledge, lateral ankle pain can be proven to be of neural origin by blocking the deep peroneal nerve proximal to the ankle. At this site, the nerve is lateral to the extensor hallucis longus and medial to the extensor digitorum longus ( Fig. 9A-6, A ). If there is not complete relief, then the sural nerve is blocked proximal to the lateral malleolus ( Fig. 9A-6, B ). The first case of sinus tarsi denervation was reported in 2002 using the technique of resecting just the fascicle that innervates this joint, identifying this by intraoperative nerve stimulation (the most medial fascicle is to the dorsal skin of the first webspace, the central fascicle causes contraction of the extensor brevis muscle on stimulation, and the lateral fascicle is the one innervating the joint).[16] In a subsequent series of 13 patients reported in 2005, there were some failures related to this partial resection of the deep peroneal nerve because of joint afferents passing also through the other fascicles.[17] The current recommendation therefore is to resect the entire deep peroneal nerve. This is accomplished through an incision located 10 to 12cm proximal to the lateral malleolus. The anterior compartment is opened with an 8-cm long fasciotomy. The deep peroneal nerve can be identified by dissecting superficial to the interosseous towards the tibia, at which point the nerve is identified with the anterior tibial vessels. A 2-cm length is resected. Immediate weight bearing is permitted. Rehabilitation is begun when the sutures are removed. In these patients, related to the initial stretch/traction injury, there already may be decreased sensibility in the dorsal first webspace and decreased bulk or weakness of the extensor brevis. These should be pointed out to the patient. The numbness present during the block should be pointed out to the patient, who must be informed that this may be permanent after the nerve is resected. The successful relief of pain should approach 90% with this approach. Examples of a patient resuming beach activities and one resuming downhill skiing after this procedure are given in Figure 9A-7 .


Figure 9A-5  Innervation of the sinus tarsi from the deep peroneal nerve occurs with a branch that arises proximal to the lateral malleolus. In 25% of patients, there is a second innervation from the sural nerve.





Figure 9A-6  Local anesthetic block of the sinus tarsi is performed by first blocking the deep peroneal nerve proximal to the ankle (A), and then, if sinus tarsi pain still is present to some degree, by blocking the sural nerve proximal to the ankle (B). (Photos courtesy Stephen L. Barrett, DPM, Phoenix, AZ.)





Figure 9A-7  Results of denervating the sinus tarsi is demonstrated in this 19-year-old who has resumed playing Frisbee on the beach (A) and in this 49-year-old who has resumed downhill skiing (B). The first patient was injured running on the beach and the second during a fall while rock climbing.



Peroneal Nerve Injuries

The peroneal nerve arises in the popliteal fossa from the sciatic nerve and travels distally around the fibular neck. There are no sites of entrapment in the popliteal fossa, although the nerve can be injured in this location iatrogenically. Figure 9A-8 illustrates the three most common sites for injury to athletes of this nerve, which consist of sites of anatomic narrowing at which the branches of this nerve are at the risk, namely, the common peroneal nerve at the fibular neck, the superficial peroneal nerve in the distal leg, and the deep peroneal nerve in structures over the dorsal ankle and foot.


Figure 9A-8  The peroneal nerve is at risk for injury in athletes because of stretch/traction and compression of the common peroneal nerve at the fibular neck, the superficial peroneal nerve as it exits the fascia in the distal third of the leg, and the deep peroneal nerve as it crosses the dorsum of the ankle and the foot. For the deep peroneal nerve, the most common site of entrapment is beneath the extensor hallucis longus tendon. These three sites are noted by arrows.  Courtesy www.DellonIPNS.com Web site, patient-interactive tutorial.


The common peroneal nerve can be injured in many athletic activities. The common mechanisms for injury include direct trauma to the knee in contact sports, such as sliding into base in baseball, football, or soccer, and stretch/traction injuries related to inversion sprains of the ankle. Positions such as catcher in baseball put the common peroneal nerve at risk from chronic compression. The most common symptoms include paresthesias into the lateral aspect of the leg and the dorsum of the foot or the perception that the leg is going to “give out.” The first symptom set is related to neural ischemia, which gives rise to the paresthesias in the reversible ischemic block degree of nerve injury. The second set of symptoms, I believe, is related to a similar phenomenon in the motor innervation of the muscles that control ankle dorsiflexion and toe extension. These symptoms are transient and worsen with activity. There may be no positive physical findings with the exception of tenderness of the common peroneal nerve at the neck of the fibula. At this stage of treatment, awareness of this diagnosis is critical, and the treatment is related to relieving pressure on the nerve by changing the athlete's workout regimen. As symptoms become more persistent, the earliest sensory change will be the pressure required to distinguish one- from two-point static touch using the Pressure-Specified Sensory Device ( Fig. 9A-9 ). Electrodiagnostic testing most likely will still be normal. The first muscle to demonstrate weakness usually is the extensor hallucis longus (see Figure 9A-9 ). With the onset of muscle weakness or the increase in distance required for two-point discrimination, the degree of compression is sufficiently chronic and severe to justify neurolysis of the common peroneal nerve. This is illustrated in Figure 9A-10. The incision is oblique at the fibular neck. Care is taken not to injure the occasionally present lateral cutaneous nerve of the calf. The fascia is opened and the common peroneal nerve identified. The nerve is followed distally to the entrapment site at the peroneus longus muscle. If there has been direct knee trauma, the fascia will be adherent to the nerve, and the neurolysis then is continued proximally into the popliteal fossa. Recent observations have made the following modifications to the procedure as previously described[18]: 20% of cadavers but 80% of patients will have a fibrous band deep to the peroneus longus muscle. This must be searched for and divided if present, and there often will be a notch at this location in the nerve ( Fig. 9A-11 ). A smaller percentage of patients also will have fibrous bands on the surface of the lateral head of the gastrocnemius muscle, deep to the nerve, and these must be released. Finally, a high origin of the soleus muscle may narrow the entrance of the nerve into the anterolateral compartment, and this origin must be released from the fibula.[19]


Figure 9A-9  Physical examination and neurosensory testing related to common peroneal nerve entrapment. (A) Weakness of the extensor hallucis longus is the first muscle to show physical findings related to the motor function. (B) Weakness or atrophy of the extensor digitorum brevis should be evaluated. Complete dropfoot is obvious. (C) Evaluation of the sensory component with the Pressure-Specified Sensory Device results in a computer printout in which the pressure required to discriminate one- from two-point static touch is measured. In this report the left, blue bars are above the 99% confidence limit for pressure for age (the horizontal black bar), indicating abnormal function for the left side, whereas the right side, in red, is below the bar. The asterisk denotes abnormal distance for the measurement, indicating axonal loss. The sensibility is abnormal for both the deep and superficial peroneal nerve, indicating either that both of these nerves are abnormal or that the location of the problem is proximal, at the fibular neck.




Figure 9A-10  Intraoperative view follows neurolysis of the common peroneal nerve. Note that the fascia superficial to the peroneus longus has been divided and is held by two clamps. The muscle has not been divided. Fascial bands deep to the peroneus longus often are present and must be divided. Similar structures deep to the nerve may be present on the lateral gastrocnemius muscle belly and should be divided. Finally, the entrance of the nerve into the anterolateral compartments must be widened. The blue vessel loop is on the sural nerve, which can be identified through this incision for the treatment of a painful sural neuroma.





Figure 9A-11  Intraoperative view of common peroneal nerve being compressed by a fibrous band beneath the peroneus longus muscle. (A) The muscle is retracted. The white fibrous edge of the band is apparent, and it extends deep to the muscle. (B) After the band is resected, the indentation or notch in the common peroneal nerve is evident.



The superficial peroneal nerve has a variable anatomy in the leg. Up to 40% of cadavers have the superficial peroneal nerve either completely in the anterior compartment ( Fig. 9A-12 ) or a branch in the anterior and a branch in the lateral compartment ( Fig. 9A-13 ). [0200] [0210] The superficial peroneal nerve exits from beneath the deep fascia to become subcutaneous in the distal third of the leg. This site is quite variable but is most commonly located 10 to 12cm proximal to the lateral malleolus (see Fig. 9A-8 ). In young athletes, such as runners or dancers, this site can be compressed because the muscles of the anterior and lateral compartment bulge during exercise, creating ischemic neuralgia. This pain goes away with cessation of the physical activity. The diagnosis should be made with compartment pressure measurements while the patient is in a controlled exercise environment, such as on a treadmill. Elevation of pressure to greater than 30mm Hg coinciding with the pain is an indication for fasciotomy. Although the fasciotomy incision does not need to be long, the fasciotomy should be extensive to prevent a small muscle herniation, which itself can be painful. The fascia is well vascularized, and its edges should be cauterized to minimize postoperative bruising or hematoma. Care is taken to not injure the nerve, and the neurolysis must be extended proximally until the nerve is surrounded by muscle and distally until the nerve enters the subcutaneous tissue (see Fig. 9A-12 ). For soccer players, this nerve can be injured directly by the ball or by being kicked. Similar injuries can occur in field hockey and lacrosse. Symptoms of chronic compression of the superficial peroneal nerve are paresthesias from the distal leg into the top of the foot, without motor symptoms. There will be a positive Tinel sign at the site of compression. Sensory testing will demonstrate normal sensibility in the dorsal first webspace and abnormal sensibility over the dorsolateral foot. Results of neurolysis of this nerve are good to excellent in 85% of patients. [0210] [0220] Surgery is performed on an outpatient basis, and immediate ambulation is encouraged to permit gliding of the nerve through the surgical site. Rehabilitation begins when the sutures are removed.


Figure 9A-12  A female catcher injured her right leg sliding into base and ultimately required a lateral ankle stabilization (A). At 3 years after her injury, and with her no longer able to play softball, she was found to have a painful sinus tarsi, a nonpainful scar, and a positive Tinel sign over both the superficial and common peroneal nerve. A block was administered to the deep peroneal above the ankle, relieving her of her sinus tarsi (lateral ankle) pain. (B) In surgery, the superficial peroneal nerve was found to be completely within the anterior compartment. This view demonstrates the fasciotomy of this compartment and complete neurolysis. (C) This view demonstrates the fascia separating the two compartments, attached to the fibular, and the small retractor lies beneath the deep peroneal nerve, to denervate the sinus tarsi.




Figure 9A-13  Intraoperative view of neurolysis of superficial peroneal nerve. In this patient, there was a branch of the nerve in both the anterior and the lateral compartment, emphasizing, as in Figure 9A-12 , the need to release both compartments.



The deep peroneal nerve has been described classically as being entrapped beneath the extensor retinaculum in front of the ankle, with this location being called the anterior tarsal tunnel, and the clinical symptoms being termed the anterior tarsal tunnel syndrome. [0230] [0240] [0250] In my experience, this is a capacious region, with the deep peroneal nerve between tendons, bone, extensor retinaculum, and fat and little chance for compression unless there has been a crush, a burn, an ankle fusion, or previous surgery (see Fig. 9A-8 ). In contrast, just distal to the inferior crus of the extensor retinaculum the extensor hallucis longus tendon crosses the deep peroneal nerve in close proximity to the base of the first metatarsal and the cuneiform. This is the area in which ganglions arise, and a dorsal exostosis forms. This exact site was described as a location of chronic nerve compression in 1990.[26] The deep peroneal nerve at this location innervates the joints of the first and second metatarsals and the cuneiform bones, and therefore symptoms of pain from the dorsum of the foot through to the plantar surface, like a “knife stabbing” this location, can occur, in addition to the aching in the forefoot and paresthesia in the webspace. This is a site that has been illustrated by Schon[2] to be a risk for ballet dancers in the pointe position and can be directly injured and the source of persistent pain following metatarsal stress fractures or Lisfranc fracture/dislocations. Tightly fitting athletic shoes have been reported to cause compression of the deep peroneal nerve, [0230] [0240] [0250] including by ski boots. [27] I have seen this to be the problem in an ice skater who had pain in this area on the take-off and landing of her spins. Loosening the laces on her skates did not help. There was a positive Tinel sign at this location. Radiographic evaluation, including MRI, had been normal. Her electrodiagnostic studies had been normal (with the more proximal anterior tarsal tunnel location, electromyogram [EMG] of the extensor brevis digitorum brevis muscle can help in the diagnosis), but her neurosensory testing with the Pressure-Specified Sensory Device demonstrated increased pressure threshold and abnormal two-point static threshold for distance. At surgery, her deep peroneal nerve clearly was indented by the extensor hallucis brevis tendon (see Fig. 9A-1, A ), and this tendon was removed. She was able to resume ice skating at 10 days and return to doing jumps and spins without pain.

Posterior Tibial Nerve Injuries

There is no “anterior tibial nerve,” and therefore some writers use the term “tibial nerve” instead of “posterior tibial nerve.” An informal survey of anatomy texts and recent publications continues to demonstrate that the most common usage is “posterior tibial nerve.” This nerve is in close proximity to the posterior tibial artery and vein, and therefore this is the name used in this chapter.

The proximal posterior tibial nerve arises from the sciatic nerve in the popliteal fossa, and there is no anatomic site of entrapment in that location, although the nerve can be injured iatrogenically here. For example, a 21-year-old college student injured her knee skiing. During her arthroscopy, the scope perforated the posterior capsule of the knee and avulsed the popliteal artery and vein and the posterior tibial nerve. After her emergent vascular reconstruction, she was referred at 3 months for nerve reconstruction. This required direct neurotization of the gastrocnemius muscles because their motor branches were avulsed, and nerve grafting to provide distal sensation to the plantar aspect of her foot. By 2 years after this reconstruction, she had active plantarflexion of the ankle and protective sensation to the plantar aspect of her foot.[28] The posterior tibial nerve continues distally to enter the distal leg by passing between a fibrous arcade formed between the two heads of the gastrocnemius and the soleus muscle. Theoretically, this can be a site of compression, and decompression at this level has been described by Baxter[1] as the “high tarsal tunnel.” I have had occasion to decompress the nerve in this region in two patients who had chronic compartment syndrome, and one of these was related to a sports injury. That patient developed an acute compartment syndrome related to a tight ski boot, which went without a proper diagnosis. When the leg was decompressed, about 48 hours later, the fasciotomy was proximal and inadequate. Muscle was debrided, and the wound skin grafted secondarily. By the time the patient was referred to me 3 years later, there was a chronic compartment syndrome associated with severe pain from the knee to the toes. There was inability to flex or extend the toes or ankle. The patient required a wheelchair and was under pain management, requiring a Duragesic patch, methadone, Neurontin, and fentanyl lollipops. The pain was relieved and all motor function recovered by carrying out a neurolysis of the tibial nerve in the calf, along with a four-compartment fasciotomy and a neurolysis of the common peroneal nerve at the knee. The superficial peroneal nerve had been divided during the original fasciotomy, requiring for the neuroma now to be resected and implanted into muscle ( Fig. 9A-14 ). However, the term “tarsal tunnel” should be reserved for a compression site in relation to the tarsal bones and not in the midcalf.


Fig. 9A-14  Neurolysis of the tibial nerve in the leg and the peroneal nerve from the knee to the ankle in a patient who had a chronic compartment syndrome. The acute compartment syndrome 3 years earlier was related to a tight ski boot (A). The initial fasciotomy was proximal and divided the superficial peroneal nerve. The extreme swelling of the common peroneal nerve proximal to the site of compression is noted in B, with the nerve encircled by the vessel loop. In C, the four compartment fasciotomy is noted, and the extensive release required to decompress the tibial nerve compression in the leg.



Tarsal tunnel syndrome was described in 1962 but remains relatively misunderstood. It is often referred to as the “carpal tunnel syndrome of the foot.” When my first patient was referred to me in about 1980, and I studied this statement, I realized that in fact the tarsal tunnel region was analogous to the forearm and not the carpal tunnel. Subsequently the appropriate relationships were published and are given in Table 9A-1 .[29] The patient with carpal tunnel syndrome would not be relieved by a forearm fasciotomy, and so an operation was designed to decompress the four medial ankle tunnels ( Fig. 9A-15). It is not appropriate to call this operation “tarsal tunnel decompression” alone because four separate tunnels are decompressed. It is confusing to speak of the tarsal tunnel as the “upper tarsal tunnel” and the medial and lateral plantar tunnels as the “distal” or “lower tarsal tunnel.” In this chapter, each tunnel is called by its correct anatomic name. Compression of the nerves in the four medial ankle tunnels can occur in an athlete through several different mechanisms. The medial ankle may be injured directly. Inversion sprains may create sufficient bruising and swelling so that the posterior tibial nerve and its branches become adherent during the immobilization of the ankle for 3 weeks, subsequently giving rise to chronic compression. Repetitive trauma can occur in runners, cyclers, those who do step aerobics, and so forth. The pronated foot theoretically is more likely to have pressure applied to the posterior tibial nerve branches, although this remains to be proven. A fracture/dislocation of the ankle or severe inversion sprain may directly contuse the tibial nerve and its branches. Swelling or blood products related to posterior tibial nerve tears or avulsion of a portion of the navicular may cause compression of the medial plantar nerve. Symptoms of tarsal tunnel syndrome include aching, paresthesias, or numbness in the heel, arch, forefoot, or toes. Nighttime discomfort is common. In time, muscle weakness and clawing of the intrinsic muscles occur ( Fig. 9A-16, A ) and the paresthesias progress to constant numbness. Electrodiagnostic testing can document this problem but has a high false-negative rate. Neurosensory testing with the Pressure-Specified Sensory Device (NK Biotechnical, Minneapolis, MN) can document this problem at an earlier stage than electrodiagnostic testing. [0300] [0310] [0320] An example of the documentation of tarsal tunnel syndrome with neurosensory testing is given in Figure 9A-16, B. Rehabilitation after decompression of the four medial ankle tunnels is critical to the success of the surgery. It should be clear that if a nerve is permitted to remain immobilized during the wound healing process, the formation of collagen in that process will result in scarring of the nerve into the surgical field, causing failure of the original neurolysis.[34] Early if not immediate mobilization of the nerve must be part of the postoperative regimen for the tibial nerve at the ankle as it is for the ulnar nerve at the elbow.[35] Although there are many reviews of tarsal tunnel syndrome, for example the one by Lau and Daniels,[36] there are no reported series larger than 68 patients, and their reported surgical results vary considerably. For example, an often-quoted study, in which long-term follow-up was obtained, reported just 44% of the patients with excellent outcomes and a 13% complication rate,[37] whereas a more recent report indicated 72% of the patients with satisfactory results but a 30% complication rate.[38] The most recent report, using outcome assessment, found 51% of the patients having a marked improvement in the quality or their life despite 85% of the patients stating they had excellent relief of their pain, with a 7% rate of complications.[39] Using the technique I described previously, a consecutive series of 87 legs in 77 patients had the four medial ankle tunnels decompressed between January of 1987 and December of 1994. The follow-up was a mean of 3.6 years. The results were 82% excellent, 11% good, 5% fair, and 2% failure.[40] Using a numerical grading scale,[41] there was a statistically significant improvement at the p < .001 level for each preoperative grade of impairment with the exception of level 10, intrinsic contracture. My experience has grown considerably in posterior tibial nerve decompression, with more than 600 procedures being listed in my computer between January 2000 and June 2005. This large experience is due, in part, to the application of this technique to relief of pain and restoration of sensation to patients with neuropathy resulting from diabetes, [0420] [0430] [0440] chemotherapy,[45] or idiopathic causes.[46] None of the patients have required repeat surgery with the previously mentioned operative and postoperative regimen. Results of an ongoing, multicenter prospective study are available online at www.neuropathyregistry.com.

Table 9A-1   -- Relationship between the four medial ankle tunnels and the nerve compression sites in the upper extremity

Sites of nerve compression

Lower extremity

Upper extremity

Tarsal tunnel


Medial plantar tunnel

Carpal tunnel

Lateral plantar tunnel

Guyon's canal

Calcaneal tunnel

Palmar cutaneous branch of median nerve tunnel[33]




Figure 9A-15  Illustration of the four medial ankle tunnels and the surgical approach for decompression. (A) The traditional tarsal tunnel is almost never the site of compression, but opening it permits neurolysis of the posterior tibial nerve, identification of any mass lesion that might be present, and identification of anomalies. (B) The fascia superficial to the abductor hallucis brevis is divided, and the branch of the medial plantar nerve that innervates the skin of the arch in this region in 50% of patients is identified and preserved. The muscle is retracted to reveal the fascial roof of the medial and lateral plantar tunnels. (C-D) Each of these tunnels is opened, and the septum between them is removed to create one large tunnel.  Courtesy www.DellonIPNS.com Web site, patient-interactive tutorial.




Figure 9A-16  Physical examination and neurosensory testing related to posterior tibial nerve compression. (A) Clawing, a sign of lateral plantar nerve compression, often is mistaken for hammertoes. In this patient with bilateral severe tarsal tunnel syndrome related to neuropathy, decompression of the four medial ankle tunnels on the right side has permitted reversal of the clawing on one side, while it remains on the other, nonoperated side. (B) Evaluation of the sensory component with the Pressure-Specified Sensory Device results in a computer printout in which the pressure required to discriminate one- from two-point static touch is measured. In this report the left, blue bars are above the 99% confidence limit for pressure for age (the horizontal black bar), indicating abnormal function for the left side, whereas the right side, in red, is below the bar. The asterisk denotes abnormal distance for the measurement, indicating axonal loss. The sensibility is abnormal for both the medial plantar nerve (hallux pulp) and the medial calcaneal nerve (heel, medial surface), indicating that both of these nerves are abnormal and that the location of the compression is in both the medial plantar tunnel and the calcaneal tunnel. The surgical approach is given in Figure 9A-15 .



Heel pain syndrome of neural origin is an important concept. Historically, heel pain was commonly was attributed to the presence of a medial calcaneal bone spur. This gave rise to medial heel pain's being related to plantar fasciitis. However, if the traditional treatment for heel pain in the athlete fails to give relief, is it possible that the pain can be of neural origin? And if so, which is the nerve along the anatomic path of which these pain impulses are transmitted? For heel pain symptoms, and especially if they are associated with poststatic dyskinesia, the treatment modalities must include strapping, stretching, changing shoes, using a heel cup, taking nonsteroidal anti-inflammatory medication, and getting a cortisone injection. The definition of “recalcitrant heel pain” varies, but if heel pain symptoms persist, it is appropriate to consider that a nerve may have been directly injured by repetitive running activities or that a nerve entrapment is due to inflammation or immobilization after an ankle or heel injury. Although x-ray and ultrasound are appropriate for bone and plantar fascia evaluation, traditional electrodiagnostic studies cannot truly measure the small medial calcaneal branches, and techniques that measure the motor or sensory component of the lateral plantar nerve have been used as surrogates.[47] The origin of pain from plantar fasciitis presumably is the periosteum, where this fascia originates from the medial calcaneal tubercle. This nerve, as I interpret the concept, is the nerve described first by Rondhuis and Huson in 1986[48] and subsequently popularized as the source of this heel pain by Baxter's group. [0490] [0500] [0510] It was Rondhuis and Huson who first gave this nerve the name “first branch of the lateral plantar nerve.” Ultimately, the nerve has come to be known as “Baxter's nerve.”[52] Anatomic studies have defined the saphenous, sural, and tibial contributions to the heel. [0530] [0540] Most recently, a detailed analysis of the posterior tibial nerve branches to the heel in 85 patients, performed in a bloodless intraoperative field with 3.5-loupe magnification, has outlined the many variations of the medial calcaneal nerve.[55] There are many patients with three or four branches that innervate the medial calcaneal region ( Fig. 9A-17 ). In many patients there is more than one branch from the lateral calcaneal nerve. The first branch of the lateral plantar nerve often is clearly not the branch carrying the pain impulses from the periosteum of the medial calcaneal tubercle. Those periosteal nerves always, ultimately, become part of the posterior tibial nerve, and most often are within the lateral plantar nerve. If the site of nerve compression is within the lateral plantar tunnel, then there will be symptoms of numbness or paresthesia present in addition to heel pain, and measurement of the medial calcaneal skin surface will identify an abnormal cutaneous pressure threshold. It is better therefore didactically to say that heel pain can be due to entrapment of a branch of the posterior tibial nerve, which usually is a branch of the lateral plantar nerve, but until the anatomy is defined at surgery, it is not possible to know which branch is the source of the pain. In a recent study,[56] approximately 40% of patients presenting with heel pain had abnormal medial calcaneal cutaneous pressure threshold measurements, and another 20% had abnormal medial plantar plus medial calcaneal nerve abnormal cutaneous pressure threshold measurements. The Pressure-Specified Sensory Device was used to make these measurements. Therefore in the patient with heel pain, there may be a neurogenic mechanism, it may be chronic nerve compression, and it can be identified by conducting an evaluation of sensibility. If the surgical approach involves just releasing the nerve to the periosteum, the approach described by Baxter, then the pain either may never be relieved or may take up to 1 year to improve. [0010] [0020] Furthermore, Baxter's approach includes an open medial plantar fasciotomy. [0010] [0020] [0490] [0500] [0510] [0520] If an ultrasound examination or MRI is normal for plantar fascial thickness and neurosensory testing is abnormal, then a plantar fascia release theoretically is not necessary. However, if the surgical approach is the same as that described previously for the four medial ankle tunnels, then all the variations of the medial calcaneal nerve can be identified, and each nerve followed and released. In my experience, this is sufficient to treat heel pain of neural origin. A confounding pain problem for heel pain is the patient who has had a medial plantar fasciotomy and who has a painful (DuVries-type) scar.[57] This may be called “failed” or “recurrent” fasciitis or heel pain when it actually is a true neuroma of one of these medial calcaneal nerve branches.[58] In this situation, the neuroma can be resected, an internal neurolysis of the medial plantar branch from the lateral plantar nerve accomplished, and the proximal end, after neuroma resection, is turned and implanted into the distal flexor hallucis longus muscle ( Fig. 9A-18 ).


Figure 9A-17  Variations in the innervation of the medial heel. There can be from one to four different nerves innervating the medial heel, with these arising in almost every conceivable variation from the posterior tibial, medial plantar, lateral calcaneal, or any combination of these.[55]




Figure 9A-18  Pain in the medial heel in the patient who previously has had a medial plantar fasciotomy may be due to a true neuroma of one of the branches of the medial calcaneal nerve(s). In this intraoperative photo, the previous Devries incision is noted with black marker. The neuroma of the calcaneal nerve is seen. This neuroma will be resected, and the proximal end of the medial calcaneal nerve will be implanted into the flexor hallucis longus muscle proximal to the ankle.[58]



Interdigital plantar nerve entrapment is the most appropriate name for the forefoot pain syndrome that athletes experience related to the common plantar nerve, the intermetatarsal ligament, and the metatarsal heads.[9] When this pain syndrome occurs to the common plantar digital nerve in the interspace between the third and fourth toe, it traditionally is termed Morton's neuroma. Repetitive impact on the forefoot in runners, people doing step aerobics or kickboxing, or those wearing athletic shoes that are too pointed are the athletic settings in which this problem may occur. The important distinction to be made is that Morton's “neuroma” is actually chronic nerve compression and not a true neuroma ( Fig. 9A-19 ). Therefore my approach to this is a neurolysis of the common plantar digital nerve through a dorsal approach.[59] The intermetatarsal ligament is completely divided, and fibrous edges to intrinsic muscles are divided. The swelling in the nerve is left alone. The nerve is left loose to shift its position in the widened space with all phases of gait. There is support for this approach now in several reports, using both an open [0600] [0610] and an endoscopic technique.[62] In more than 50 patients, I have not had to take a patient back to surgery to resect this nerve (unpublished observations). I have one failure so far in a patient with a painful neuropathy of unknown etiology who remained with forefoot pain after the neurolysis and probably was a poor choice to have only the interdigital neurolysis. This raises the concept of the “double crush” phenomenon, [0630] [0640] [0650] in which a proximal site of compression renders the distal nerve susceptible for compression, as well. In the posterior tibial nerve region, entrapment of the posterior tibial nerve branches in the medial ankle region will reduce the gliding of the interdigital nerve system, rendering them more susceptible to compression. Each patient with a clinical interdigital nerve compression must be evaluated for a coexisting neuropathy or tarsal tunnel syndrome by measuring the sensibility of the hallux pulp, heel, and dorsal foot surface. It is possible that patients with an interdigital nerve compression in a webspace other than the third have a proximal nerve compression site. For patients with more than one interdigital nerve compression, the adjacent webspaces can be approached through a single incision, as noted by Schon,[2] and our preferred incision for this is given in Figure 9A-20 .[66] Although relief of interdigital nerve compression usually can be achieved by inserting a metatarsal bar into the shoe, changing the shoebox to incorporate a wider toe, administering nonsteroidal anti-inflammatory medications and cortisone injections, persistent pain requires surgical treatment. Repetitive cortisone injections may weaken the capsule of the metatarsophalangeal joint or induce tendon or volar plate rupture. The results of resecting the common plantar interdigital nerve can approach 90%, [0670] [0680] [0690] but failure results in a true neuroma, the correction of which requires a plantar approach and implantation of the resected interdigital nerve into muscle in the arch of the foot. [0060] [0080]


Figure 9A-19  Interdigital nerve compression. The common plantar nerve must glide beneath the intermetatarsal ligament during the initiation of gait. It can become compressed in this area between the metatarsal heads (left). The swollen nerve may appear to be a neuroma(right), but, in the absence of direct, not repetitive, trauma, it is not a true neuroma. Neurolysis by division of the intermetatarsal ligament instead of nerve resection is recommended (left). Resection creates a true neuroma. It often is stated that this occurs most commonly in the third interspace because the formation of the third interdigital nerve from both the medial and lateral plantar nerves restricts gliding of this common plantar digital nerve; however, there is great variability in the formation of this nerve.  Courtesy www.DellonInstitutes.com Web site, patient-interactive tutorial.



Figure 9A-20  Interdigital plantar nerve compression can occur in adjacent webspaces. This incision permits entry into each webspace, avoiding parallel incisions.[59] In this patient, whose foot was crushed, there was an interdigital nerve compression in each interspace. On the left, the incisions are seen at 2 weeks after surgery and on the right 6 months after surgery. Note that the incision is centered over the metatarsal, and the distal end of the incision then goes off into each interspace.



Less Common Lower-Extremity Peripheral Nerve Problems

The lateral femoral cutaneous nerve usually is depicted as being below the inguinal ligament and about 2cm medial to the anterior superior iliac crest. Athletes who fall directly on the anterior iliac crest may have pain related to such a “hip pointer” injury. This may occur in wrestling during a takedown, in football during a tackle, or in rugby. Numbness in the anterior and lateral thigh and anterior hip pain can be the result of acute and then chronic compression of this nerve ( Fig. 9A-21 ). This problem was known decades ago as meralgia paresthetic or a painful thigh. Because this nerve can extend to the lateral surface of the knee, it can even present as knee pain, which I have seen in a slim, female, long-distance biker. In biking, the repetitive hip flexion/extension can cause irritation of this nerve, especially when it is located within the inguinal ligament and adjacent to the anterior superior iliac crest. Indeed, this nerve is so commonly found in this location at surgery ( Fig. 9A-22 ), that it prompted a cadaver study, reported in 1995.[70] This demonstrated that more than one third of cadavers have this nerve located within the inguinal ligament and adjacent to the bone or the origin of the sartorius muscle. Patients with this nerve compression have discomfort sitting up straight and often will be observed to be sitting in the examining room with the affected leg slightly extended at the hip. Neurosensory testing of the lateral versus the medial thigh skin can document the present of this nerve compression, which is difficult to identify with electrodiagnostic testing.[71] In the acute situation, it is important to administer anti-inflammatory medication and use methods to reduce the swelling while maintaining gliding of the nerve so it does not become scarred. Ultrasound with steroid iontophoresis may be helpful in the subacute phase. If the symptoms have been present for more than 6 months and cannot be relieved by massage or by wearing clothes without a tight belt, then surgical decompression must be considered. The results of neurolysis of lateral femoral cutaneous nerve have been reported showing excellent results in more than 80% of patients.[72]


Figure 9A-21  Groin pain of neural origin can be evaluated by considering the skin territory innervated by each nerve, shown in different colors, below. The surgical incisions that are responsible for creating neuroma and pain syndrome of these nerves also are shown. The lateral femoral cutaneous nerve has a large territory, and most often this nerve has chronic compression, rather than a true neuroma. Its territory extends to the knee, and compression of this nerve can give rise to knee pain in athletes with repetitive hip flexion, such as cyclists. Pain in the groin after hernia repair is the usual cause of the painful neuromas in the other territories.  Courtesy www.DellonInstitutes.com Web site, patient-interactive tutorial.



Figure 9A-22  Intraoperative view of neurolysis of the right lateral femoral cutaneous nerve. This nerve is located adjacent to the anterior superior iliac crest. The narrowed area of the nerve is clear after division of the inguinal ligament. The neurolysis must continue proximally dividing the internal oblique fibers until the superficial circumflex iliac vessels is reached.



Hernia repair in athletes can cause pain in the groin related to either tightening of the inguinal ligament sufficient to cause compression of the lateral femoral cutaneous nerve or iatrogenic injury to the ilioinguinal and iliohypogastric nerves.[72] The typical pain pattern (skin innervation territory) for each of these nerves is given in Figure 9A-21 . Pain from a neuroma of the ilioinguinal or genitofemoral nerve may be confused with pain from tendinitis of the origin of the gracilis muscle or other adductors from the pubic ramus.

The saphenous nerve can be compressed in the midthigh in the adductor canal. This is a rare entrapment. [0730] [0740] [0750] I have seen it in the setting of cyclists who have fallen and have had bruising in the thigh and in motorcycle riders who have fallen and in whom the bike has compressed the midthigh. This also has been observed in a martial artist as a stretch/traction problem. If this does not resolve, the surgical approach requires a large midthigh incision and division of the fascia between the rectus lateralis and the adductor group of muscles ( Figure 9A-23 ).



Figure 9A-23  Adductor canal syndrome. This patient had an injury to the left knee and thigh. Previous operations resected the infrapatellar branch of the saphenous nerve, but the patient had persistent pain in the saphenous distribution. With the leg abductor and externally rotated at the hip, a positive Tinel sign was present at the site of the adductor canal, which has been exposed (A). The saphenous nerve is encircled with a vessel loupe (B). For chronic compression, a neurolysis is sufficient. If there is a distal pain syndrome, the saphenous nerve can be resected at this level and implanted into an adductor muscle.



The sural nerve can be entrapped theoretically where it exits the fascia in the distal lateral calf. Its surgical anatomy has been described well, and the variability of the location for the lateral sural joining the medial sural is significant.[53] A stretch-traction injury to the sural nerve in this distal location has been described, but it is rare.[76] More likely, the athlete will have had a direct injury to this nerve from sports trauma,[77] or the nerve will be injured iatrogenically related to a lateral ankle surgery.


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Further reading

Dellon AL: Deciding when heel pain is of neural origin.  J Foot and Ankle Surgery  2001; 40:341-345.


B B. Plantar heel pain

Lew C. Schon,Florian Gruber,
Glenn B. Pfeffer

Plantar heel pain is one of the most common foot problems in the athlete/dancer. Running, cutting, pivoting, and jumping, especially on unyielding surfaces, places tremendous, acute, and repetitive stresses on the heel. Often it is difficult to determine the exact etiology of the heel pain because several different underlying problems can occur simultaneously with symptoms. The complex anatomy of the heel challenges the practitioner to distinguish among several potentially pathologic structures that lie within a small area. The difficulty in establishing the specific etiology and subsequently reversing underlying processes correlates with the complexity of achieving a cure.

Focal causes of plantar heel pain include the following:



Fat pad insufficiency



Plantar fascial rupture



Insertional plantar fasciosis



Midsubstance plantar fasciitis



Nerve entrapment: (a) tarsal tunnel syndrome and (b) first branch of the lateral plantar nerve



Stress fracture of the calcaneus




In differentiating these diagnoses, a comprehensive physical examination and medical history are essential. Knowing the onset of the pain (e.g., acute trauma vs. overuse) and the precipitating activity is useful to establish etiology. The exact location, character (i.e., musculoskeletal or neuritic), and duration of pain should be noted. The relationship of pain to a particular action or a specific activity modification is useful for realizing a diagnosis and treatment plan. The history should include an overview of the patient's general medical and orthopaedic conditions to determine whether there is systemic or more global musculoskeletal disorder contributing to the local problem. Radiculopathy in the L5-S1 distribution should be considered in a patient with back pain, and a peripheral neuropathy ruled out when heel pain is diffuse, nonfocal, and bilateral. The seronegative arthropathies should be considered in an athlete with bilateral heel pain.[1] Chronic pain at rest is an unusual presentation for plantar heel pain, and if a neurologic cause is not responsible, a tumor of the calcaneus should be considered.

Fat Pad Insufficiency

With each heel strike, the calcaneal fat pad cushions the foot and body from direct and potentially catastrophic impact. A healthy, middle-aged man has a gait velocity of approximately 82m/minute and a cadence of 116. This rate results in 58 heel strikes per minute with a force of up to 110% of body weight. A sprinter does not place a direct increased stress on the heel, but a middle- or long-distance runner may generate a force of up to 200% of body weight. Considering timing, impact forces, and average heel pain area (23cm[2]), the loading pressure of a 70-kg man is approximately 9.3kg/cm[2] when he is running.

Anatomic studies of the human heel pad have identified structural specialization capable of withstanding these high loads.[2] The anatomy of the heel pad was first described by Tietze in 1921.[3] He emphasized the specialized anatomy of the heel pad, with elastic adipose tissue organized as spiral-formed, fibrous tissue septa anchored to one another, the calcaneus, and the skin. Designed to resist and absorb compressive loads, the tissue septa are U-shaped or comma-shaped fat-filled columns with a vertical orientation. The septa are reinforced internally with elastic transverse and diagonal fibers that connect the thicker walls and separate the fat into compartments or cells. The thickness of the heel pad is the most important factor in determining the stresses seen in the tissues beneath it.[4] After age 40, the adipose tissue usually begins to deteriorate gradually, with the insidious loss of collagen, elastic tissue, water, and overall thickness of the heel pad. The result is an inescapable softening, flaccidness, and thinning in the heel pad and a concomitant loss of shock attenuation. Some patients experience these changes earlier because of genetic factors.

An athlete with heel pain secondary to fat pad incompetence usually complains of diffuse plantar heel discomfort aggravated by sports on harder surfaces, such as a basketball court, concrete floors, or cinder track. By clinical examination the patient has a soft, flattened heel pad that allows easy palpation of the calcaneal tubercles. Sometimes the pad has a particularly small surface area or thickness. Compression of this area by the examiner duplicates the symptoms, with pain maximal over the central weight-bearing portion of the heel pad overlying the bone. Initially there is no radiation of the pain, and the plantar fascia is not tender. The area of maximal tenderness is proximal and central on the heel ( Fig. 9B-1 ). With prolonged duration of the condition, patients may develop calcaneal stress fractures, fasciitis/fasciosis, or local neuralgia.


Figure 9B-1  Focal causes of plantar heel pain.



The only intervention for this condition is avoidance of high-impact activity, especially on unyielding hard surfaces, using a cushioned heel cup and/or shock-absorbent footgear. A plastic or silicone heel cup that elevates the heel may be helpful both by protecting the painful area and by shifting some of the weight bearing more anteriorly. Cross training with swimming or biking is useful in maintaining physical condition while avoiding the offending activity. Avoidance of cortisone injections for this condition limits further atrophy. There is no surgical treatment for this condition.

Insertional Plantar Fasciosis

The most common site for plantar heel pain is where the plantar fascia and intrinsic muscles arise from the medial calcaneal tuberosity on the anteromedial aspect of the heel ( Fig. 9B-1 ). During sports activities, particularly long-distance running, the plantar fascia is placed under repetitive traction, which contributes to high stresses at the bone-fascia junction. The plantar fascia arises predominantly from the medial calcaneal tuberosity and inserts distally through several slips into the plantar plates of the metatarsophalangeal joints, the flexor tendon sheaths, and the base of the proximal phalanges of the digits. [0830] [0840] When the metatarsophalangeal joints are dorsiflexed with running or jumping, the inelastic plantar fascial fibers place traction on the calcaneus.[5] Typically with recurrent stresses the junction of two structures with different biomechanical properties will be the site of stress concentration. This is particularly true in the heel, where the plantar fascia, which is strong under traction or tension stresses, meets the calcaneus, which is strongest in compression load.

Over time, microtears can occur in the plantar fascia near the medial calcaneal tuberosity. A reparative response develops, along with continued traumatic fatigue in the fascia. Surgical biopsy specimens of the origin of the plantar fascia in athletes with chronic heel pain reveal collagen necrosis, angiofibroblastic hyperplasia, chondroid metaplasia, and matrix calcification. Thus it is appropriate to use the term “fasciosis” to reflect a degenerative process, rather than “fasciitis,” an inflammatory process. Periostitis of the medial calcaneal tuberosity often occurs in conjunction with degenerative changes in the plantar fascia, causing a positive delayed technetium-99 bone scan in the majority of painful heels.[7]

Because of the close proximity of the medial calcaneal tuberosity and the origin of the plantar fascia, it is not possible to differentiate clinically a fascial or bony source of an athlete's pain. Both structures usually are involved, much like other insertional tendon and fascial conditions.[8] Patients may have local, soft-tissue swelling and focal tenderness over the medial calcaneal tuberosity directly and the plantar fascia distally for several millimeters. The examiner often must apply a considerable amount of pressure to localize the painful area. Interestingly, patients almost never have increased pain or duplication of symptoms with passive dorsiflexion of the toes, which causes traction on the plantar fascia by the Windlass mechanism ( Fig. 9B-2 ). Associated tightness of the Achilles tendon is commonly seen with this condition, because limited ankle dorsiflexion places increased stress on the plantar fascia.


Figure 9B-2  Windlass mechanism.



Insertional plantar fasciosis is insidious in onset and is seen most often as an overuse condition of long-distance runners.[8] In athletes with an acute onset of symptoms, rupture of the plantar fascia should be considered[9] ( Fig. 9B-3 ). Rupture is much less common than chronic insertional plantar fasciosis and easily can be differentiated on the basis of physical examination and history. A palpable defect in the plantar fascia is present when a rupture occurs, and often there is ecchymosis. The fascia will be less taut with a rupture than with fasciosis. An old partial rupture of the plantar fascia can present with a palpable nodularity in the fascia near the medial calcaneal tuberosity and a lower arch.


Figure 9B-3  Rupture of plantar fascia.



Athletes with insertional plantar fasciosis usually experience symptoms during the first minutes of walking, especially in the morning when first out of bed. The pain gradually decreases. Discomfort is intensified by athletic activity, especially jumping or running. Some athletes have symptoms only during periods of prolonged running. It is not unusual for athletes to complain of heel pain that occurs only during the first few miles of a workout. No clear correlation between insertional plantar fasciosis and pes planus or pes cavus has been established. A positive correlation with obesity exists, although most athletic patients do not have this concern. A lateral x-ray of the heel will exclude a stress fracture or tumor of the calcaneus. Even among high-performance athletes, a stress fracture is extremely rare.

Leg lengths always should be examined when evaluating athletes with chronic heel pain. If one leg is longer than the other, often there is a history of repeated injury to the shorter leg. Heel pain is seen more often in the shorter leg and may be treated effectively with an appropriate lift. A functional short-leg syndrome can result from running on the same tilt of road or in the same direction on the track. In both instances, after many miles of training, one heel will be more stressed than the other. By using both sides of the road or intermittently changing directions on a training track, stress between both heels can be equalized.

The cornerstone of conservative treatment in athletes is modification in training. Mileage reduction, alternating activities, work reduction, and shortened workouts should be considered.[10] Low-resistance cycling and swimming pool running are effective cardiovascular activities that usually are not stressful to the heel. Oral anti-inflammatory agents, contrast baths, ice massage, and soft-soled shoes or sneakers also are used. Plantar fascia stretching exercises should be instituted. If the athlete has Achilles tightness, this should be stretched as well.

A study of 101 patients (complete data for 66 patients) with symptoms longer than 10 months compared a specific plantar fascia stretching program (group A) with an Achilles stretching program (group B) for 8 weeks. [0890] [0900] Patients in both groups used full-length, prefabricated orthoses. Patients in group A were instructed to perform a stretch by placing the affected foot on the thigh of the contralateral leg. While hyperextending the toes with the ipsilateral hand until a stretch in the arch is felt, the contralateral hand palpates the degree of tension of the plantar fascia. This position was held for 10 seconds and repeated 10 times. The plantar–ascia-stretching group was advised to perform the stretching before any weight bearing. All patients in the other group were instructed to stretch three times a day.

After this treatment period, the Achilles tendon group was given the plantar fascia-specific stretching protocol. The results were evaluated after 8 weeks and 2 years. At 8 weeks the plantar–fascia-stretching group had significantly fewer complaints of pain at its worst and pain at the first steps in the morning. At the 2-year follow-up, there was no statistically significant difference between the groups. After 2 years, 94% reported less or no pain and 58% reported no pain. The majority of patients (62%) achieved the best results within the first 6 months.

Low dye taping and a one-eighth-inch medial heel wedge may be added in an attempt to reduce the stress on the plantar fascia. A night splint ankle-foot orthosis with the ankle fixed in 5 degrees of dorsiflexion also may be indicated. Using this technique, Wapner et al.[13] had a 79% success rate after an average of 4 months of splint use. In refractory cases, a short-leg cast for 2 to 6 weeks followed by a custom-made orthosis may help break a painful cycle. An off the shelf boot brace typically is not helpful in this condition because the orthosis tends to concentrate the stresses on the heel.

In athletes with refractory symptoms, a steroid injection often is beneficial. Care should be taken to inject the steroid deep to the plantar fascia so as not to cause atrophy of the fat pad. A medial approach of the injection is best used so that the steroid can be spread along the broad origin of the plantar fascia. A 25-gauge needle is walked across the anterior border of the calcaneus just deep to the plantar fascia, thereby avoiding the plantar nerves ( Fig. 9B-4 ). Two to three milliliters of an equal mixture of lidocaine, bupivacaine, and long-acting steroid should be administered. Multiple steroid injections may predispose the athletic patient to plantar fascia rupture and should be avoided.[14] A majority of patients respond to these conservative measures. A patient may have some persistent symptoms for up to 6 months, but usually only 4 to 6 weeks will be lost from training or competitive athletics if treatment is started early.


Figure 9B-4  A steroid injection from the medial side of the heel. To avoid steroid-induced atrophy of the fat pad, the solution is injected deep into the plantar fascia. The heel spur arises within the origin of the flexor digitorum brevis muscle.



Extracorporeal shock wave therapy (EWST) has been introduced for the treatment of chronic plantar fasciosis. Alvarez[15] reported on the use of high-energy shock wave before surgical management is considered. The safety and early preliminary efficacy of the high-energy shock wave using the OssaTron was evaluated. Twenty heels of 20 patients were treated with 1000 extracorporeal shock waves from the OssaTron to the affected heel after administration of a heel block. Each patient underwent an extensive evaluation, including x-ray, KinCom, physical examination, and a 10-cm visual analog scale. Of the 20 patients treated, 17 were improved or pain free. There were no complications or adverse effects attributed to the procedure. Zingas and colleagues[16] also studied the safety and efficacy of musculoskeletal shock wave therapy in 29 patients with chronic plantar fasciitis. In this study the patients were enrolled in a randomized, 1:1 allocated, placebo-controlled, prospective, double-blind clinical study with two groups: one receiving ESWT with the Dornier Epos Ultra and the other receiving sham treatment. The authors concluded that shock wave therapy is useful in the treatment of chronic plantar fasciitis that has failed conventional conservative methods. The Food and Drug Administration now has approved this treatment for chronic plantar fasciitis, but only some insurance plans cover the treatment. The decision whether to use high-energy or lower-energy shock wave also has been debated. To date there is no consensus on how to define the terms high-dose and low-dose shock wave.

An advantage of the lower energy machine is that the patient does not need general anesthesia or an invasive nerve block to tolerate the procedure. An advantage of the high-energy machines is that typically only one treatment is required, as opposed to three for the lower-energy machines. Different therapy-regimens seem to result in different efficacy of treatment. In 2003, Speed et al.[17] found no significant difference between the treatment and placebo group. In their study the authors applied shock waves (0.12mJ/mm[2]) monthly for 3 months. The authors concluded that efficacy may be highly dependent on machine types and treatment protocols.

Porter et al.[18] concluded that ESWT was less effective than a single corticosteroid injection in patients who underwent a standardized Achilles tendon and plantar fascia stretching program. Kudo et al.[19]found significantly better outcome of an ESWT group in comparison with a placebo group 3 months after treatment. Treatment consisted of approximately 3800 total shock waves (±10) reaching an approximated total energy delivery of 1300mJ/mm[2] (ED+) in a single session versus placebo treatment. Several studies focusing on the durability of pain relief show good results for EWST for chronic plantar fasciitis for follow-up times from 2 to 6 years. [0980] [0990] Further research is needed to develop evidence-based recommendations for using ESWT for treatment of this condition.

A recent therapeutic approach for plantar fasciitis is local injection of botulinum toxin A. Placzek et al.[22] performed a pilot study with 25 patients using a single subfascial injection of 100 units of botulinum toxin A in the first 6 patients to determine the optimal treatment dose and with 200 units in the other 19 patients. The group that received 200 units reported a substantial reduction of maximal and continuous pain 2 and 14 weeks after the injection and no signs of muscular weakness in a clinical exam. Babcock et al.[23] presented a randomized placebo-controlled, double-blind study of 27 patients (43 feet). They applied 40 units at the tender area at the medial tuberosity of the calcaneus and 30 units between an inch distal of the heel and the middle of the foot. The placebo group received injections with the same volume of saline. Main outcome measures included the pain visual analog scale, Maryland foot score, pain relief visual analog scale, and pressure algometry response. Patients were assessed before injection, at 3 weeks, and at 8 weeks. The botulinum group improved significantly in all measures and showed no adverse side effects.

Another possible treatment option for enthesopathies that has been used for patients with elbow tendinosis involves injection of platelet-rich plasma (PRP). Mishra and Pavelko[24] studied 20 patients with persistent pain for a mean of 15 months despite conservative therapy. The pain level measured with a visual analog scale from 0 to 100 was 82 on average (60‐100). Fifteen patients received a single percutaneous injection of PRP. The control group (n = 5) got an injection with bupivacaine. Eight weeks after treatment, the patients in the PRP group had a 60% improvement in visual analog scores and the control group showed only 16% improvement (p = .001). Only the platelet-injection group could be observed in further follow-up. At 6 months and at final follow-up after a mean 25.6 months (range, 12‐38 months), 81% and 93% of these patients noted improvement in their pain visual analog score. The authors concluded that PRP injection reduces pain significantly in their patient group. Research is needed to determine whether this result is applicable to treatment of plantar fasciitis.

In those few patients who fail prolonged, conservative treatment, surgical release of the plantar fascia should be considered. However, every attempt should be made to avoid this procedure in competitive athletes. Release of the plantar fascia may have a detrimental effect on function. Daly et al.[25] demonstrated in their study a change in both arch height and the ratio of arch height to arch length following a plantar fascia release. A less energetic pattern of walking following a plantar fascia release also was seen. Further, if the plantar fascia is divided surgically, increased compressive forces are transmitted to the dorsal aspect of the midfoot, with decreased flexion forces on the metatarsophalangeal joint complex.[6] These changes can lead to dorsal midfoot pain and metatarsalgia postoperatively ( Fig. 9B-5 ).


Figure 9B-5  If the plantar fascia is divided surgically, there are increased compressive forces transmitted to the dorsal aspect of the midfoot and decreased flexion forces on the metatarsophalangeal joint complex.



If surgery is performed, it is necessary to discuss the role of the spur with the patient. In general, resection of the heel spur is not performed because it does not contribute to the pathophysiology. In addition, resection of the spur can lead to a slightly more aggressive release of the fascia to gain exposure and may lead to some more bleeding because of the presence of raw bone. On the other hand, at times the spur is quite large and the patient is fixated on its presence. It can be easier to remove the spur than to explain at each visit that the pain that remains while he or she is healing is common and will resolve. It is useful to advise the patient that the heel spur arises deep to the plantar fascia in the nonweight-bearing substance of the flexor brevis muscle and therefore is probably not involved in producing the pain. Most patients are informed that the calcaneal spur was of great importance in the treatment of heel pain historically. They also are told that many patients without heel pain have spurs and that many patients without spurs have pain. Tanz[26] demonstrated that only 50% of patients with plantar heel pain had a heel spur and that 16% of nonpainful heels also had a heel spur. Rubin and Whitton[27] determined that only 10% of patients with heel spurs were symptomatic. Finally they are told that the spur can be left alone, but that they still can have successful conservative or surgical treatment for the plantar fasciitis. Lapidus and Guidotti[28] showed that the successful treatment of heel pain was not contingent on the surgical removal of a heel spur and concluded that plantar calcaneal spurs do not cause the painful heel, as they have been postulated to do. We leave the decision about spur resection to the surgeon's discretion.

Surgical technique

Plantar fascia release may be performed using a regional anesthetic with intravenous sedation and a standby general anesthetic. An ankle block is highly useful, using a 1:1 solution of 0.25% bupivacaine hydrochloride (Marcaine) and 1% lidocaine, both without epinephrine.

An oblique incision is begun along the inferomedial aspect of the heel, just anterior to the calcaneus where the inferior abductor fascia joins the medial plantar fascia ( Fig. 9B-6 ). This 2.5- to 4-cm incision is planned anterior to the medial calcaneal branch of the posterior tibial nerve, avoiding inadvertent division of the nerve and the formation of a painful postoperative neuroma. Care should be taken to search for this nerve branch during the operative approach because its course can be more anterior than expected.


Figure 9B-6  Incision used to release the plantar fascia. The incision may be extended along the nonweight-bearing aspect of the foot.



Using blunt dissection, the medial edge of the plantar fascia origin is visualized easily. Isolate the fascia from the adipose tissue, which lies inferiorly, and the fascia of the abductor hallucis muscle, which lies superiorly. If necessary, the incision can be extended a few centimeters transversely across the nonweight-bearing aspect of the sole.[29] A Freer elevator is used to isolate the plantar fascia along its origin on the calcaneus. The plantar fascia often will be thickened in this area from chronic changes. A scalpel then is used to divide the plantar fascia as it arises from the calcaneus. Any degenerated portions of the plantar fascia should be excised. Typically a piece of fascia is removed measuring 3 to 4mm wide and a thickness of 2 to 4mm. The depth of the release should be 4 to 5mm.

If a heel spur is present in the origin of the flexor brevis muscle, it easily can be removed using a small osteotome and rongeur. Care should be taken not to remove cortical bone of the calcaneus and thereby create a stress riser. A reciprocating rasp works well for both gross reduction and final smoothing of the calcaneal surface. One should protect the first branch of the lateral plantar nerve (nerve to the abductor digiti quinti), which runs across the heel just deep to the heel spur and the flexor brevis muscle. If a tourniquet is used, it should be deflated and hemostasis obtained. A bulky compression dressing is used, and the patient is instructed not to bear weight for 3 to 4 days to allow for wound healing. After the fourth day, weight bearing can progress as tolerated using crutches.

Minimal incision surgery is not recommended for release of the plantar fascia. Direct visualization of the plantar fascia is required to gain an adequate release, and inadvertent division of the medial calcaneal sensory nerve easily can occur when an incision of 1cm or less is used. Benton-Weil reported on percutaneous plantar fascia release in a retrospective study with 35 patients using a questionnaire and the visual analog score at an average follow-up time of 34 months. He described improvement of the visual analog score from 8.2 to 2.1. In 83% the results of the procedure met or exceeded the patient's expectations.

An interesting technique that has been used for plantar fasciosis involves drilling the calcaneus. Some authorities add this to their surgical protocol when there is any suspected calcaneal stress fracture, determined on the basis of a hot bone scan or tenderness along the wall of the calcaneus. Schon uses this method as an adjuvant for these cases but at times has drilled only the calcaneus and had good results. Hassab and El-Sherif[30] drilled the os calcis to obtain relief of recalcitrant heel pain. They performed 68 operations in 60 patients and reported excellent results in 62, good in 2, and poor in 4. Santini et al.[31] presented a retrospective study of 25 feet in 21 patients treated with drilling of the calcaneus. The indication was chronic heel pain in combination with increased uptake in the delayed bone scans. Under local anesthesia, three holes were drilled in the medial cortex of the calcaneus. After an average follow-up time of 21 months, the authors noted a decrease in pain from 8.8 (4-10) preoperatively and 2.4 (0-10) using the visual analog score. Six of seven patients who had another bone scan postoperatively showed resolution of the increased uptake. The outcome was worse in patients with rheumatoid and other systemic diseases and Haglund deformity. Santini states that his results of calcaneal drilling are comparable to other surgical options for treatment of chronic heel pain.

Endoscopic plantar fascia release is another method for treating this condition. The technique was first popularized by Barrett and Day,[32] who proposed this technique as causing less tissue damage than open treatment. In a follow-up, multicenter study of 652 procedures, they reported 62 complications in 53 patients but felt that it afforded satisfactory results. O'Malley and associates[33] reviewed the surgical results following endoscopic plantar fasciotomy in 16 patients (20 feet) with an average preoperative duration of symptoms of 4 years. Nine had complete relief of pain, and another 9 feet were improved. One patient with bilateral symptoms had no relief in either foot. The average American Orthopaedic Foot and Ankle Society hindfoot score improved from 62 to 80, a statistically significant difference. Patients with unilateral symptoms did better than those with bilateral symptoms. There were no iatrogenic nerve injuries.

Other authors have reported various complications from endoscopic plantar fascial release, including stress fractures,[34] pseudoaneurysm formation,[35] and recurrence of pain.[36] A prospective study by Saxena[37] compared uniportal endoscopic release of the medial 50% of the plantar fascia in athletes versus nonathletes. All patients had undergone at least 8 months of conservative treatment. Good and excellent results were reported in all 16 athletically active patients using the Modified Plantar Fascia Score (MPFS) and an average return-to-activity time of 2.6 months. Of the 10 patients in the control group (at time of surgery 12 years older than athletic patients), 5 had poor outcome. All of the control patients had a body mass index (BMI) higher than 27.

Most authors believe that only the medial one half or medial two thirds of the plantar fascia be released because of the high incidence of lateral foot pain following more aggressive release.

Entrapment of the First Branch of the Lateral Plantar Nerve

One of the most commonly overlooked causes of chronic plantar heel pain in the athlete is entrapment of the first branch of the lateral plantar nerve [1160] [1170] [1180] ( Fig. 9B-7 ). The first branch innervates the periosteum of the medial calcaneal tuberosity, the long plantar ligament, and the abductor digiti quinti and flexor brevis muscles.[41] Entrapment of the nerve accounts for approximately 20% of chronic heel pain. Entrapment occurs as the nerve changes from a vertical to a horizontal direction around the medial plantar aspect of the heel ( Fig. 9B-8 ). The exact site of compression is between the heavy, deep fascia of the abductor hallucis muscles and the medial caudal margin of the medial head of the quadratus plantae muscle (see Fig. 9B-9 ). Athletes who spend a significant amount of time on their toes, such as sprinters, ballet dancers, and figure skaters are prone to entrapment of the first branch of the lateral plantar nerve by the well-developed abductor hallucis. The medial calcaneal nerve branches that innervate the plantar medial aspect of the heel pass superficial to the abductor hallucis muscle and are not involved with entrapment of the first branch. Another potential site of entrapment of the first branch is the point at which the nerve passes just distal to the medial calcaneal tuberosity.[40] Inflammation and spur formation in the origin of the flexor brevis muscle can produce sufficient swelling to cause compression of the nerve against the long plantar ligament ( Fig. 9B-10 ). The inflammatory changes of heel pain syndrome (HPS) therefore can predispose to chronic entrapment of the nerve.


Figure 9B-7  First branch of the lateral plantar nerve.




Figure 9B-8  Entrapment of the first branch of lateral plantar nerve occurs as the nerve changes direction from vertical to horizontal around the medial plantar aspect of the heel.




Figure 9B-9  Site of compression of the first branch of the lateral plantar nerve.




Figure 9B-10  The plantar fascia is retracted. The first branch of lateral plantar nerve is exposed (arrow). A large heel spur is marked (S).  From Kenzora JE: The painful heel syndrome: an entrapment neuropathy, Bull Hosp Joint Dis 47:178, 1987.


The diagnosis of entrapment of the first branch of the lateral plantar nerve is made on the basis of clinical grounds. It therefore is incumbent on the examiner to differentiate first-branch entrapment from other, more common causes of heel pain ( Fig. 9B-11 ). Early-morning pain is not as prominent with nerve entrapment, which tends to cause pain more at the end of the day or after prolonged activity. The pathognomonic sign of entrapment of the first branch of the lateral plantar nerve is maximal tenderness where the nerve is compressed between the taut deep fascia of the abductor hallucis muscle and the medial caudal margin of the quadratus plantae muscle. Chronic inflammation of the plantar fascia may predispose to entrapment of the first branch of the lateral plantar nerve. The patient therefore may have some tenderness over the proximal plantar fascia and medial calcaneal tuberosity. Without maximal tenderness over the course of the nerve on the plantar medial aspect of the foot, however, the diagnosis of entrapment should not be made (see Fig. 9B-1 ). Some patients may have paresthesias elicited with pressure over the nerve at the entrapment site, although this does not occur commonly. Entrapment of the isolated medial plantar nerve, “jogger's foot,” occurs more distally at the level of the navicular tuberosity and should not be confused with entrapment of the first branch of the lateral plantar nerve more proximally.


Figure 9B-11  Entrapment of nerve to the abductor digiti quinti.



Motor weakness in the abductor digiti quinti muscle may on occasion be detected, although no cutaneous sensory deficit occurs. Electromyography and nerve conduction studies are not yet consistent in diagnosing entrapment of the first branch of the lateral plantar nerve.[42] Measurement of nerve conduction slowing across the site of entrapment is technically demanding, and denervation potentials in the intrinsic foot muscles may occur only rarely because of the possible dynamic nature of this particular compression neuropathy. A comparison may be drawn to the diagnosis of a posterior interosseous nerve entrapment in the upper extremity.

Treatment for athletes with entrapment of the first branch of the lateral plantar nerve is similar to that of HPS, with rest, nonsteroidal anti-inflammatory agents, contrast baths, ice massage, physical therapy, and steroid injection serving as the foundation for conservative care. A shock-absorbent viscoelastic heel insert also will help to decrease inflammation in the area. In athletic patients with excessive pronation, especially long-distance runners, a nonrigid, mediolongitudinal arch support can decrease compression of the nerve.

In 1984, Baxter and Thigpen[39] presented the first large clinical series of patients treated operatively for entrapment of the first branch of the lateral plantar nerve. Twenty-six patients with 34 involved heels underwent operative decompression; 82% of the patients experienced complete relief of their symptoms. In 1992, Baxter and Pfeffer[38] published a series of 69 heels in 53 patients with chronic heel pain who had surgical release of the first branch of the lateral plantar nerve. The average duration of heel pain symptoms was 23 months. No patient had fewer than 6 months of conservative treatment before surgery. The average duration of preoperative conservative treatment was 14 months. Postoperatively 61 heels (89%) had excellent or good results. The average follow-up was 49 months. Approximately half the patients in Baxter's second study developed heel pain as a result of a sports activity, usually long-distance running. Other activities included aerobics, basketball, volleyball, and tennis. Eighty-five percent of this group had good or excellent results from surgery. The mean recovery time of the athletic subgroup to resumption of sports activities was 3 months. This amount of time was not considered excessive, given the mean of 23 months of preoperative symptoms.

Surgical Technique

The surgical approach to release the first branch of the lateral plantar nerve should be from the medial side of the heel. The patient is supine on the operating table. No tourniquet is required, although an ankle tourniquet can be used. A 4-cm oblique incision is made on the medial heel over the proximal abductor hallucis muscle. The incision is centered over the course of the first branch of the lateral plantar nerve. The medial calcaneal sensory nerve branches are not encountered as they course posterior to the incision. Care is taken, however, to preserve any aberrant branches.

The superficial fascia of the abductor hallucis is divided with a no. 15 blade, and the muscle is retracted superiorly using a Ragnell retractor. A section of deep fascia of the inferior abductor hallucis is removed directly over the area where the nerve is compressed between this taut fascia and the medial border of the quadratus plantae muscle. A small portion of the medial plantar fascia may be removed to facilitate exposure and clearly define the plane between the deep abductor fascia and the plantar fascia. The deep fascia of the abductor hallucis then is divided from inferior to superior to sufficiently free the nerve from entrapment. If present, a heel spur is removed, using a Freer elevator to protect the nerve that runs superiorly. The abductor hallucis muscle belly and its superficial fascia are left intact. A plantar fascia release is not performed unless the patient has been symptomatic over the plantar aspect of the medial calcaneal tuberosity and direct visualization provides evidence of pathology in the proximal portion of the plantar fascia.

At the end of each case, a small hemostat is used to palpate along the course of the nerve to make sure it is free from any adhesions proximally or distally. The wound is closed with interrupted horizontal mattress nylon sutures. No subcutaneous sutures are used. A bulky dressing is placed. Patients are allowed to bear weight in a postoperative shoe as tolerated and to gradually return to sports activities after 3 to 4 weeks.

A plantar heel spur forms in the insertion of the flexor brevis muscle on the calcaneus. The first branch of the lateral plantar nerve courses from medial to lateral directly above this muscle. Although it is unlikely that a heel spur is a direct mechanical cause of plantar heel pain, inflammation in the area of the spur is a theoretical source of compression of the first branch of the lateral plantar nerve as it passes above the spur. A heel spur, if present, therefore should be excised. Care should be taken when excising the spur to protect the first branch of the lateral plantar nerve. The plantar fascia should not be divided to preserve its biomechanical advantage during sports activities.

Tarsal Tunnel Syndrome

Another nerve entrapment capable of producing chronic heel pain is tarsal tunnel syndrome. Posttraumatic adhesions, bony spurs, chronic inflammation, benign tumors, and varicosities all can all cause compression of the posterior tibial nerve within the tarsal tunnel. Excessive pronation in a long-distance runner may predispose to tarsal tunnel syndrome by placing repeated stress on the structures on the medial side of the heel. Hindfoot varus, in association with excessive pronation, also may be associated with tarsal tunnel syndrome.

The salient clinical feature of tarsal tunnel syndrome is direct focal tenderness over the nerve as it passes beneath the flexor retinaculum. Percussion of the nerve in this area will reproduce the patient's symptoms, which can include pain, burning, or tingling on the plantar aspect of the foot. Subjective numbness of the toes may occur, although objective decreased sensibility is rarely demonstrated. Some patients may complain of proximal radiation of their symptoms. Electromyography and nerve conduction studies can be helpful in making a diagnosis. A normal study, however, does not exclude the diagnosis of tarsal tunnel syndrome. In general, the plantar heel pain produced by tarsal tunnel syndrome is more diffuse and less focal than that of either HPS or entrapment of the first branch of the lateral plantar nerve. A careful clinical examination should easily distinguish among these three entities.

A medial heel wedge will decrease tension on the nerve. Steroid injection into the tarsal tunnel also may be beneficial but usually produces only transient relief of symptoms. Surgical release of the flexor retinaculum and exploration of the tarsal tunnel can be expected to provide relief of symptoms in 90% of athletic patients. Decompression of both the medial and lateral plantar nerves into the midfoot should be performed in any patient with preoperative tenderness along the course of these nerves ( Fig. 9B-12 ). Internal neurolysis of the nerve is rarely indicated.


Figure 9B-12  Decompression of medial and lateral plantar nerves into the midfoot should be performed in any patient with preoperative tenderness along the course of the nerves.



Midsubstance Plantar Fasciitis

Tenderness over the plantar fascia in the midfoot is aptly called midsubstance plantar fasciitis. This condition presents with tenderness over the midportion of the plantar fascia. As opposed to insertional plantar fasciosis, dorsiflexion of the toes almost always exacerbates the patient's symptoms by the Windlass mechanism stretching the midfascial fibers ( Fig. 9B-13 ). There is usually is only minimal tenderness over the most proximal fascial fibers, which are painful in insertional plantar fasciosis. Plantar fasciitis is seen more often in sprinters and middle-distance runners, who spend more time on their toes during athletic activity.


Figure 9B-13  Dorsiflexion of the toes causing tension on the plantar fascia. The symptoms of true plantar fasciitis are reproduced with this maneuver.



Tendinitis of the flexor hallucis longus tendon can present with pain in the plantar medial midfoot. This condition can be distinguished easily from plantar fasciitis. Passive dorsiflexion of the great toe aggravates both plantar fasciitis and flexor hallucis longus tendinitis, but resisted flexion of the toe is painful only with involvement of the tendon. Careful palpation with motion of the tendon usually is sufficient to confirm the diagnosis. A painful plantar fibromatosis involving the midplantar fascia also can be detected by careful examination.

A mediolongitudinal arch support often is not tolerated in a patient with plantar fasciitis because it pushes up on the plantar fascia and increases tension on its fibers. Circumferential taping of the foot with 1-inch adhesive tape applied over a nonadhesive elastic wrap usually is beneficial. Rest, alteration of training, nonsteroidal anti-inflammatory agents, ice massage, contrast baths, and physical therapy, including ultrasound and plantar fascial stretching, also are indicated. A one-eighth-inch medial heel wedge may take tension off the plantar fascia. If these modalities fail, the cornerstone of treatment is the University of California Biomechanics Laboratory (UCBL) orthosis.[43] The theory of the UCBL orthosis is to hold the foot in a position that relieves tension on the plantar fascia. The orthosis accomplishes this reduction in tension by holding the heel in inversion and applying forces against the navicular and lateral aspect of the forefoot, without direct pressure on the soft tissue underneath the longitudinal arch. The UCBL insert usually is not helpful in patients with insertional plantar fasciosis because the rigid material used in constructing the insert often aggravates the inflamed heel. It is extremely unusual to operate on a patient for true midfoot plantar fasciitis. If prolonged, conservative treatment of more than 6 months fails, however, a similar operative approach to that used for insertional plantar fasciosis is indicated.


Ninety-eight percent of patients with heel pain can be treated successfully with conservative treatment. If treatment is begun soon after the onset of symptoms, most athletes can minimize their downtime to 6 weeks or less. Understandably many athletic patients are reluctant to give up or significantly modify their sports activities. They continue to train through the pain and thereby establish a chronic and refractory condition. In those few patients who require surgery, an excellent result can be obtained if the correct diagnosis is made and the surgeon addresses the specific cause of the athlete's plantar heel pain.

Case Study 1  

A 23-year-old, nationally ranked middle-distance runner had chronic heel pain. She failed all conservative treatment, including prolonged physical therapy, heel cups, an orthotic device, and shoe modification. She did not want to use a cast. She had maximal tenderness over the medial plantar hindfoot consistent with the diagnosis of entrapment of the first branch of the lateral plantar nerve. Her symptoms had been present for 1 year. Under regional anesthesia she had a surgical release of the deep abductor fascia, freeing up the nerve. Her plantar fascia was left intact. Six weeks later she resumed training with complete relief of pain.

Case Study 2  

A 44-year-old, competitive long-distance runner had 2 years of heel pain consistent with insertional plantar fasciosis. His mileage had decreased from 80 miles per week to 0. Under regional anesthesia through an oblique medial incision his plantar fascia was released. No heel spur was present. His plantar heel pain gradually resolved over 4 months. He returned to 40+ miles per week.

Case Study 3  

A 23-year-old, male volleyball player was seen for a second opinion regarding chronic heel pain. Surgery had been recommended. The diagnosis was midfoot plantar fasciitis. He wore a rigid, plastic orthotic device, which did not help. The orthotic device was discarded and circumferential taping of the midfoot over a nonadherent wrap was begun. He began a program of physical therapy three times a week to stretch the Achilles tendon and plantar fascia and decrease inflammation. A nonsteroidal anti-inflammatory agent, ice massage, and contrast baths also were used. His symptoms sufficiently improved so that surgery was not required.

Case Study 4  

A 24-year-old, female, long-distance runner had a plantar fascia release. Postoperatively she developed metatarsalgia and dorsolateral midfoot pain. She was seen in consultation after repeated attempts at conservative treatment failed to relieve her midfoot pain. Her plantar heel pain had resolved after surgery. She required 8 weeks of casting to alleviate the midfoot symptoms.

Case Study 5  

An aerobics instructor was seen for chronic hindfoot pain following a plantar fascia release. A longitudinal incision had been used. A small portion of the medial heel was numb. A neuroma in the superficial medial calcaneal nerve was identified. Symptoms persisted despite two steroid injections into the neuroma. The nerve was resected surgically to its origin within the tarsal tunnel. The patient experienced continued tenderness at the nerve ending. Another patient with a similar problem developed a reflex sympathetic dystrophy that remained refractory to conservative treatment.


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