The achilles tendon can sustain either acute traumatic or chronic overuse injuries depending on the mechanism of injury. An acute strain of the achilles tendon results from a rapid tensile stress placed on the tendon that causes tissue disruption (Fig. 11.2). Like the ankle sprain, this injury is graded as mild, moderate, or severe. Achilles tendinopathy is prevalent and potentially incapacitating in athletes involved in running sports. It is considered to be a degenerative, not an inflammatory condition (Kader et al 2002). Severe cases may respond to conservative care, but sometimes require surgical intervention. However, mild and moderate cases will respond to conservative care using the PRICES protocol. In addition, the use of temporary heel lifts will relieve some of the tensile stress in the tendon during recovery. If a heel lift is to be used it is important to note that there should be a lift of equal size under both extremities to avoid an artificial leg length inequality and potential injury to the joints further up the kinetic chain.

Figure. 11.2 Medial Achilles tendon stress due to rearfoot valgus.

The exact aetiology and pathogenesis of tendon pain is not fully understood (Alfredson 2005; Shalabi et al 2004) and is undergoing much research at present. Recent studies have shown that there may be a genetic predisposition to suffering from a tendinopathy (Harvie et al 2004; Kannus & Natri 1997). Multiple intrinsic and extrinsic risk factors have been associated with achilles tendon injuries; suggesting this condition is complex and interactions between gene–gene and gene–environment are probably involved in the aetiology of these conditions (September et al 2007).

In association with tendon degeneration, there appears to be signs of neural inflammatory markers in nerves in close proximity to affected tendons (Hart et al 1995). The well-known neurotransmitter and potent modulator of pain in the central nervous system, glutamate, is found in high levels in painful tendons, but not in normal tendons (Alfredson et al 2001). In conjunction with neurovascular ingrowths into painful tendons as demonstrated by Bjur et al (2005), there is now evidence that neural pathways and neovascularization are associated with the pain of tendinopathy rather than just a simple case of tissue degeneration.

There appears to be a lack of research consensus on the efficacy of management of this achilles tendinopathy, but the lack of suitable evidence in support of a given management method does not necessarily imply a lack of clinical effectiveness (Andres et al 2008).

The following interventions have been demonstrated as providing clinical effectiveness:

• Mechanical conditioning—Tendons respond to mechanical forces by adapting metabolism and structural reorganization (Hampson et al 2008). Tenocytes respond by altering gene expression patterns, protein synthesis, and cell phenotype to enhance healing (Wang 2006).

• Eccentric loading—The best evidence to date demonstrates that eccentric exercises are likely to be a useful management for achilles tendinopathy, but is insufficient to suggest it is superior or inferior to other forms of therapeutic exercise (Rompe et al 2007).

The initial occurrence of an achilles tendon strain can subsequently result in chronic strains and/or tenosynopathy. When this occurs, the practitioner must consider the possibility of an underlying biomechanical weakness contributing to the chronicity of recurrent achilles tendinopathies. Chronic achilles tendinopathy (CAT) may result from chronic overuse of the tendon as a result of an underlying biomechanical weakness in foot and ankle function. Excessive and prolonged pronation through the rear foot is an example of this type of underlying biomechanical foot fault. As a result, the calcaneous undergoes excessive eversion during the gait cycle, causing a valgus stress through the medial aspect of the calcaneus and the distal attachment of the achilles tendon. This ultimately results in pain, oedema, and sometimes crepitus from overuse of the tendon and yields a tendinopathy. This overuse injury may be resolved with the use of the PRICES protocol, but will be recurrent if there is an underlying biomechanical weakness. The preferred option for the management of this condition is the addition of foot orthoses to the treatment plan (Alfredson & Lorentzon 2000). There is a further discussion of foot orthoses in the management of chronic overuse syndromes in the foot and ankle at the end of this chapter.

Plantar fasciitis

The plantar fascia is a connective tissue that is a cross between a tendon and a ligament. It attaches to the bottom of the heel and then spans the length of the foot, spreading out like a fan to connect with the distal metatarsals, as shown in Fig. 11.3. The function of the plantar fascia is to support the medial longitudinal arch (MLA) and control the pronation of that arch during normal gait.

Figure 11.3 Plantar fascia.

When abnormal pronation occurs, the plantar fascia is repetitively and excessively stressed, causing a pain in the arch of the foot that is felt most keenly on the plantar and medial aspects of the calcaneus, at the calcaneal tubercle, although this pain can also extend along the full length of the foot. On histological examination, Lemont et al (2003) found increased fibroblasts, ground substance, and vascularity, but not significant inflammatory mediators.

In the light of any objective findings, including calf muscle length, talocrural hypomobility, forefoot pronation, and heel pain, treatment is encouraged to include a multifaceted approach that addresses underlying anatomical and biomechanical conditions (Dyck & Boyajian-O’Neill 2004). This can be the case with either an overpronated or oversupinated foot (Souza 2001); a classic sign of this condition is severe pain on walking in the morning that dissipates once the patient is up and moving about.

Plantar fasciitis (PF) is very common among runners, walkers, aerobic dancers, and athletes involved in jumping sports. Its onset can be triggered by changes in the surface used for training or competition (e.g. from track to grass or vice versa), or a change in footwear. Another common trigger for PF is a change in training; the addition of hills, stairs, or sprints, for example, can cause overuse of the plantar fascia, leading to inflammation and injury. The patient will often report an increase or change in walking habit, over longer distances, wearing inappropriate footwear, or a change of walking surface (i.e. carpet to hardwood flooring).

If a patient develops PF for the very first time as a result of these changes in activity, the condition will usually respond readily to standard treatments. However, a recurrence of the condition despite treatment suggests that there is an underlying mechanical fault. The mechanism is similar to that discussed above and involves excessive or prolonged overpronation that causes stress to the plantar fascia at the calcaneal attachment.

In addition to the PRICES protocol for the relief of symptoms, spray and stretch techniques that block the reflex spasm and sensation of pain have also been shown to be effective in the conservative treatment of PF. Other techniques, such as cross-friction, ischaemic compression, heat, and manipulation, are effective on their own, or in combination with the spray and stretch technique. Considering the referral pattern of trigger points (TrPts) of the gastrocnemius/soleus to the foot, passive stretching of these muscles leads to a better prognosis and reduces the likelihood of recurrence. Acupuncture has also shown to be effective with treatment of TrPts associated with PF (Steinmetz 1999). Taping techniques have been shown to be one of the most reliable and effective short-term treatments if used correctly. These can also be used to predict the success of orthotics and are important indicator of the specific goals of orthotic therapy (Cornwall & McPoil 1999). The inclusion of functional orthotic therapy (FOT) has been demonstrated to be an effective addition to management plans for acute and chronic PF (Bartold 2004; Dimou et al 2004; Martin et al 2001).

Metatarsalgia and Morton’s neuroma

Pain in the forefoot is often associated with, and is a precursor to, Morton’s neuroma. The patient will initially experience the insidious onset of forefoot pain that gets progressively worse if it goes untreated. If the condition is allowed to progress, this will eventually result in connective tissue formation (scarring) around the peripheral nerves of the foot, predominantly in the nerves between the second, third, and fourth digits of the foot. The patient may then experience paraesthesia in the toes along with secondary forefoot pain, referred to as entrapment neuralgia (Souza 2001).

The standard treatment involves the PRICES protocol with the addition of a metatarsal pad placed under the metatarsal arch to relieve pressure on the soft tissues between the distal metatarsals (Hassouna & Singh 2005; Nashi et al 1995). Footwear modifications may be required (e.g. a wider shoe) and wearing high-heeled shoes should be discouraged.

It is interesting to note that the underlying mechanism of this overuse injury is associated with overpronation through the rearfoot, midfoot, and forefoot changing the functional biomechanics of the metatarsal arch (Michaud 1997). Once again the incorporation of FOT along with pain management strategies can facilitate enhanced recovery.

Anterior and posterior tibial tendinopathy

Pain on the anterior or posterior aspect of the tibia is commonly referred to as ‘shin splints’. The posterior tibial muscle and tendon are attached along the posterior and medial aspect of the tibia, passing posteriorly to the medial malleolus and underneath the MLA and attaching to the plantar aspect of the tarsal bones of the foot, allowing it to support the MLA like a stirrup. The anterior tibial muscle and tendon are attached along the anterolateral aspect of the tibia and insert into the superior aspect of the mid-tarsal bones. When the muscle and tendon contract, there is a lifting of the superior aspect of the tarsal bones that contributes to the support of the MLA.

When the MLA overpronates excessively, there is a consequent overstretching of the anterior and posterior tibialis muscles and tendons. The muscles and tendons exert tractional stress along the attachments to the tibia, causing disruption of the soft tissues of the tendon as well as the periosteum of the bone. Chronic irritation will eventually lead to a stress fracture of the tibia, secondary to the chronic stress on the periosteum. Clinically, this causes palpatory pain, particularly in the lower third of the tibia.

This type of injury is common in long-distance runners, but it is also frequently seen in other sports, especially those that involve jumping. As with PF, if an athlete develops this condition for the very first time following abrupt changes to training surfaces or methods, the problem will respond readily to standard treatment. However, if the condition is unresponsive to treatment, or recurs subsequently, then there may well be an underlying biomechanical weakness in the foot that will benefit from the inclusion of FOT in the treatment plan.

Bilateral asymmetrical pronation syndrome

The inquisitive practitioner will note that these overuse injuries are often unilateral, or at least worse on one side. Why then, when the patient presents with one of these overuse injuries, does this asymmetry occur? As they were walking or running with both feet, there must be an inherent asymmetry in the joint mechanics that predisposes one extremity to become symptomatic over the other.

As noted above, many of these conditions are secondary to overpronation of the rear foot, medial longitudinal arch, or forefoot, secondary to faulty foot mechanics. The diagram in Fig. 11.4 demonstrates how rear foot and forefoot varus deformity present in the non-weight-bearing phase of the gait cycle becomes a valgus stress as the foot and ankle go from an inverted to everted position with weight-bearing. When this occurs repetitively, excessively, or for a prolonged period during a single gait cycle, the result is overuse of the soft tissues.