Posterior Ankle Impingement-Pathoanatomy, Assessment and Management

Background

Posterior ankle impingement (PAI) is an umbrella term for a collection of pathologies that cause posterior ankle pain with ankle plantarflexion (pointing the toes downwards). PAI most commonly presents in athletes participating in sports involving end range or forced plantarflexion such as; ballet, soccer and cricket fast-bowlers.

Figure 1: Common examples of sports that require repetitive loaded ankle plantarflexion.

In these athletes, end range plantarflexion is painful and limited due to impingement of soft tissue or bony structures between the bones at the back of the ankle.

Anatomy

The talocrural and subtalar joints are complex structures that rely on multiple passive (ligaments, joint capsules, and bony congruency) and dynamic (muscles) supports for optimal stability and function.

We will briefly dive into the specific anatomy of the structures involved in PAI here:

Talocrural (ankle) joint

The talocrural joint (TCJ) consists of the distal fibula and tibia (shin), and the proximal (upper) surface of the talus. It is a hinge joint, responsible for ankle dorsiflexion and plantarflexion (pointing toes up and down). The TCJ is lined with a thin loose capsule and is supported by many ligaments- of relevant interest are the posterior talofibular and posterior tibiotalar (forming the posterior aspect of the deltoid ligament) ligaments.

Figure 2: Bony anatomy of the talocrural joint.
Figure 3: The posterior tibiotalar and talofibular ligaments are potential sources of PAI

Talus and subtalar joint

The talus is situated between the mortise (created by the distal tibia and fibula) and the calcaneus (heel) bone. Posteriorly, the talus features two tubercles- medial and trigonal processes. These form a groove that houses flexor hallucis longus (FHL), which is responsible for big toe flexion. The medial and trigonal processes can also be implicated in bony PAI- these will be discussed in detail later.

Figure 4: Posterior aspect of the talus and calcaneus. A: medial tubercle. B: groove for FHL. C: trigonal process.

The articulation between the talus and calcaneus forms the subtalar joint, which allows inversion and eversion of the rearfoot. It is lined by a thin, loose synovial capsule.

Mechanisms of PAI

PAI can be classified as bony or soft tissue impingement. As you can see in figure 4, many structures can be compressed at the back of the ankle with end range plantarflexion. Here we will take a look at the most frequently seen causes of PAI- these can occur in isolation or in combination:

Table 4: Possible soft tissue and bony structures that can be compressed in the space between the distal posterior tibia and posterosuperior aspect of the calcaneus.

Trigonal process (Postero-lateral tubercle) of the talus

Variation of the trigonal process of the talus is the most common cause of bony related PAI symptoms.

Os trigonum is a small accessory bone that forms around the age of 8-13, and fuses with the trigonal process by the age of 17 in approximately 80% of the population¹. In the other 20% it articulates with the talus via cartilage synchondrosis (connected by hyaline cartilage). Os trigonum related PAI is likened to a nut-cracker, whereby the ossicle becomes wedged between the posterior tibia, talus and calcaneus towards end of range plantarflexion.

Trigonal process fracture can result from acute trauma (forced hyper-plantar flexion) or chronic microtrauma, leading to PAI. These can cause mechanical irritation of the surrounding soft tissues, further contributing to symptoms. Lastly, an elongated posterolateral talar tubercle (known as a Stieda’s process) can also be implicated with PAI.

Figure 5: Presence of os trigonum on lateral X-ray.

Other less common causes of PAI include a prominent calcaneal tuberosity, fracture of the posteromedial talar tubercle and other accessory ossicles.

Soft tissue causes

Flexor Hallucis Longus

FHL pathology is the most common cause of soft tissue PAI¹, and is frequently seen in ballet. The FHL is a deep muscle arising from the posterior surface of the fibula, coursing through the medial and trigonal processes of the talus and attaches to the plantar surface of the big toe.

Tenosynovitis occurs when the synovial sheath surrounding the tendon becomes irritated and inflamed with repetitive loading through large ranges of motion. Tendinopathy occurs when repetitive loading exceeds the tendon’s capacity to adapt, resulting in tendon thickening, pain and reduced elasticity.

It is important to note the presence of FHL pathology can occur in isolation without PAI. However, tendon changes associated FHL pathology are frequently involved with soft tissue PAI.

Figure 6: Moving from plie to pointe works FHL through full range of motion

Ballerinas moving in and out from a flat foot plie position to en pointe load the FHL muscle tendon complex through extreme range. Eccentric overload (e.g. landing jumps), weak calf musculature and excessive pronation can all increase FHL loading. Presence of os trigonum can also compress and irritate the tendon^2,3.

The associated tendon and synovial sheath changes may reduce space at the back of the ankle and lead to impingement.

Posterior capsuloligamentous and cartilage pathology

Scarring, thickening and inflammation of the subtalar joint capsule can develop after acute trauma or repetitive overload. Similarly, the cartilage lining the joint articulations can become damaged. These cartilaginous and capsular changes can become impinged.

Laxity of the ATFL, one of the lateral stabilisers of the ankle joint, may permit excessive forward translation of the talus on the tibia⁴. This allows the posterior surface of the talus to come into closer contact with the posterior lip of the tibia, thereby increasing the risk of PAI.

Other less common sources of PAI include accessory muscles (e.g. peroneus quartus and flexor digitorum accessories longus), cysts and ganglions⁵.

Video summary of PAI causes:

Diagnosis

Presentation

Athletes will present with posterior ankle pain deep to the Achilles tendon with plantarflexion. Symptoms worsen with activities that require repeated or loaded plantarflexion. It usually presents in athletes that place or load their ankle into the extremes of this position, and is therefore uncommon in the general population.

Typical aggravating factors include rising up onto toes, downhill running⁶, cutting and change of direction, high heel shoes, and kicking in ball sports. Cricket fast-bowlers also place significant loads through a relatively plantarflexed lead plant foot when delivering.

Overuse vs chronic PAI

Approximately half of PAI cases present as overuse injuries from repetitive microtrauma, and the other half stemming from acute traumatic injuries⁷.

Typical acute injuries include lateral ankle sprains and forced hyper-plantarflexion.

After acute ankle injury, symptoms can be delayed and often take up to 3-4 weeks⁶ to manifest, usually very gradually. This can be attributed to the early inflammatory response that causes localised pain and swelling, restricting ankle ROM. Once this settles and plantarflexion range of motion improves, the resulting soft tissue or bony pathology becomes symptomatic.

Overuse injuries may stem from:

• Repetitive loading of the ankle resulting in cartilage defects, ligament laxity, capsule synovitis and degenerative changes.
• Load exceeding FHL tendon capacity resulting in tenosynovitis and tendinopathic changes.

Subjective findings to listen closely for include:

• Increases in training load (especially pointe or jumping work in ballet)
• Specific mechanism of injury involving loaded or extreme plantarflexion
• Previous history of ankle joint/FHL injury or chronic ankle instability
• Pain with activities requiring end range plantarflexion
• Restricted movement into plantarflexion

Objective examination

Observation

Depending on the nature and chronicity of PAI, swelling may be observed.

Swelling on the medial aspect of the ankle joint, just under the medial malleolus can suggest FHL involvement, which needs to be differentiated from other pathologies. Ligamentous injury and subtalar synovitis may also contribute to posterior ankle swelling.

Assessing arch height is important as it can be a contributory factor in PAI.

Pes cavus (high rigid arch) feet have poor shock absorption when planting the foot, predisposing athletes to bony or joint related PAI.

Conversely, pes planus (flat) feet require greater contribution from the musculature (such as FHL and tibialis posterior) and ligaments (e.g. spring ligament) to maintain the arch. These foot types make athletes more susceptible to soft tissue variations of PAI, especially FHL tenosynovitis.

Functional assessment

Careful assessment of plantarflexion and aggravating movement patterns are important considerations for both an accurate diagnosis and management. Ballet dancers with limited plantarflexion range may invert at the heel to compensate for reduced height when moving into pointe position. There can be increased rotary forces and strain on posterior ankle structures during turnout due to lack of hip external rotation⁸. Therefore, hip external rotation strength and range should be assessed in dancers presenting with PAI. Fast bowlers that overstride on their plant foot increase ankle and subtalar joint loading.

Figure 7: Inverting at the rearfoot in an attempt to increase height can increase strain on ankle structures and predispose dancers to PAI.

Strength testing

Inadequate strength of the triceps surae complex (gastrocnemius and soleus) and intrinsic foot muscles (such as flexor hallucis brevis, adductor and abductor hallucis) can overload the FHL. Athletes should be able to perform at least 20 single leg calf raises with good form- this means maintaining a straight knee, keeping the midline of the shin in line with the 2^nd metatarsal, no rocking forwards for momentum, smooth controlled movements at a speed of 1 second up- 1 second down through full range of motion. Sue Mayes, principle physiotherapist for the Australian ballet company found that dancers with <25 single leg heel raises were more likely to report ankle pain in the previous 6 months, and had a substantial decline in time-loss ankle injuries after a SLHR training program.

Sound intrinsic foot muscle control is especially important for ballet dancers. These muscles assist in flexing the big toe (and do not cross the ankle joint)- offloading the overworked FHL during pointe work or jumping/landing.  They also help protect and stabilise the arch of the foot, reducing the risk of other ankle injuries.

Figure 8: The Australian Ballet Company’s guide to performing single leg heel raises with perfect technique

Palpation

Maximal pain and tenderness is felt deep to the Achilles tendon and may be slightly medial or lateral. FHL tenosynovitis is usually accompanied by palpable swelling and crepitus (which can be auscultated on a stethoscope) over the medial aspect of the ankle.

Posterior impingement test with overpressure

This test involves placing the ankle joint into maximal plantarflexion with the patient in prone. Overpressure with inversion/eversion bias can be applied for less irritable patients. It is commonly accepted as the definitive test for PAI although there is limited evidence on its specificity or sensitivity.

POSTERIOR PLANTAR FLEXION IMPINGEMENT TEST

Range of motion

Active and passive plantarflexion range of motion will be generally painful in PAI. Rapid, repeated or forced plantarflexion are likely to reproduce symptoms in less irritable athletes. Dancers with limited ankle plantarflexion range of motion are more likely to compensate by inverting at the heel to achieve increased height. This increases the risk of inversion injury, FHL overuse and PAI.

Ankle dorsiflexion and 1^st MTP extension range of motion can help identify associated muscle tightness and joint hypomobility. This can alter joint biomechanics during sport activities, predisposing athletes to PAI.

Integrity of the ATFL can be assessed using the anterior drawer test. This should be considered in athletes with a previous history of ankle sprain because excessive anterior movement at the talus can lead to PAI (outlined under Posterior capsuloligamentous and cartilage pathology).

FHL testing

Resisted big toe flexion is a good way of isolating the FHL to screen for weakness and pathology. A variation of this test specific to FHL’s function involves simultaneous resisted big toe flexion and ankle plantarflexion through full range of motion. Flexing and extending the big toe may reproduce crepitus along the tendon sheath.

Differential diagnoses

There are many structures that can cause pain at the back of the ankle, which makes differential diagnosis important for management and return to sport.

Isolated FHL tendinopathy

Athletes with isolated FHL tendinopathy will typically have more pain landing from jumps compared to PAI, and should have no pain on posterior impingement testing/ maximal passive plantarflexion.

Achilles tendinopathy

These will be tender directly over (rather than deep to) the mid portion or insertion of the Achilles on the calcaneum. Achilles tendinopathy is associated with morning stiffness, warm up phenomenon, and aggravated deep stretching into dorsiflexion (especially insertional AT), setting it apart from PAI. They will not have a positive posterior impingement test.

Peroneal tendinopathy

This can be easily differentiated with pain, weakness or sublaxation on resisted dorsiflexion and eversion as well as careful palpation over the tendon.

Tarsal tunnel syndrome

Entrapment of the posterior tibial nerve in the tarsal tunnel will cause burning, tingling or numbness on the medial aspect of the ankle and plantar foot. Approximately half of cases are idiopathic, however, it may arise after significant ankle trauma such as an inversion sprain. Sensory changes and a positive Tinel’s test (tapping the posterior tibial nerve) to elicit symptoms differentiates it from PAI.

Lumbar spine radiculopathy

Radicular pain from the lumbar spine is a less likely cause of posterior ankle pain and can be easily differentiated with a neurodynamic testing that tensions the involved nerves (positive straight leg raise or slump test). Similarly, sural nerve pathology can be differentiated with a straight leg raise with inversion bias to specifically tension the nerve. PAI athletes will test negatively and have full lumbar range of motion.

Posterior tibial tendon pathology

These will present with medial ankle pain, similar to FHL pathology. Maximal tenderness is typically just behind and below the medial malleolus. They will have pain on resisted inversion, however, should have no symptoms with resisted big toe flexion or passive big toe flexion and extension.

Imaging

Standard X-rays are most often used as the first line investigation to differentiate between bony and soft tissue associated PAI. Lateral views will generally pick up an enlarged postero-lateral talar tubercle (Stieda process), os trigonum, osteophytes or loose bodies. Recent studies have found that rotating the ankle into 25degrees of external rotation⁶ provides better diagnostic accuracy for bony abnormalities of the posterior talus.

CT scans provide greater detail in respect to the size, number and location of bony lesions such as avulsion fractures.

MRI is the preferred method of imaging for evaluating soft tissues such as FHL, accessory muscles, cartilage lesions, bone marrow oedema, joint effusion and synovitis.

Management

Video summary of management

First line management of PAI should be conservative and include:

1. A period of modified workload avoiding provocative end range plantarflexion to help settle symptoms and any present swelling. The duration will largely depend on the irritability and nature of symptoms. This time is a great opportunity for athletes to cross-train and work on factors contributing to their PAI. For example, working on technique, hip external rotator and foot intrinsic strength in ballet. Field sport athletes may be able to continue running, however, should avoid change of direction or tackling or kicking. Strength and conditioning work can be continued in the gym with appropriate modification to avoid provocative positions- activities such as cycling and most above the knee strengthening exercises should be tolerated.
Of quick note, athletes with tolerable symptoms that wish to continue their season can maintain training volume. However, it is likely they will require a period of longer rest at the completion of the season. Elite athletes may opt for localised ultrasound guided corticosteroid injection to reduce swelling and pain. A lateral approach is usually performed to avoid the medial neurovascular bundle.

2. A short course of NSAIDs to reduce pain and swelling associated with PAI.

3. Mobilisation exercises or manual therapy if indicated in the objective examination. Examples may be gentle distraction and mobilisation (caution with acute subtalar joint injury) of the talocrural and subtalar joints to optimise load distribution during plantarflexion. Big toe mobilisation and soft tissue release of tight calf musculature can be performed if there are ROM deficits on testing.

4. Gradual return to activity and loading through plantarflexion range once symptoms have settled. Focused strengthening of calf and foot intrinsic muscles are critical for optimal loading and biomechanics at the ankle joint. It will help offload typically overworked muscles such as FHL and tibialis posterior.
The flexor hallucis brevis is of importance as it helps stabilise the big toe during push off and landing jumps. Deficits in FHB strength results in these propulsive and impact forces being distributed to other tissues in the foot, ankle and calf.
Ensuring proper technique with calf raises (as outlined in strength testing) is crucial for all weight-bearing athletes. Gradually progress range, ensuring that athletes tolerate symptoms during and after exercise.

The following provides a general guide to progressing exercises into an athlete’s training program.

Foot intrinsic and ankle stability exercises should be incorporated early in the rehab progress and continued on a regular basis:

• Toe yoga
• Short foot and resisted toe flexion (Theraband) with hip hinge
  
• Towel scrunches
• TheraBand big toe flexion (FHL)
• TheraBand inversion
• TheraBand eversion
• Stability board/ Mobo board/ unstable surface (add hip hinge, upper body movements)
• Y balance test protocol
• Tibialis anterior strengthening for fast bowlers is also important to help eccentrically control rapid plantarflexion in the lead leg.

Gradual loading into plantarflexion should be performed once symptoms have settled. Emphasis should be on single leg exercises to prevent ‘cheating’ with the unaffected side. Avoid ‘locking the ankle out’ at end range plantarflexion- instead focus on smooth and controlled recruitment of calf musculature, minimising excessive inversion with simple heel raises. Perform exercises from this stage onwards every other day, selecting the greatest resistance possible whilst ensuring sound technique.

• Single leg heel raise off a step
• Smith rack heel raise
• Smith rack heel raise (bent knee)
• Soleus bridge (add heel raise)
• Rearfoot elevated squat with heel raise (progress to toes on step)
• Bent knee heel raise with rear foot elevated
• Heel raise Inversion bias (TheraBand)
• Heel raise Eversion bias (TheraBand)
• Prowler sled pushes
• Weighted farmers walks (on toes and rising up onto toes)
• Horizontal resisted toe walk

Once the athlete is able to achieve >20single leg heel raises with sound technique and no increase in symptoms, they are ready to progress to more sport specific exercises. These be gradually introduced, monitoring symptoms closely, and be performed fresh. Progress from double to single leg, then add external load as required. Special emphasis should be on controlling landings and maintaining good trunk control.

• Stair climbing/bounding (progress to multiple stairs at a time)
• Skipping (progress to side to side)
• Single leg squats on slant board
• Vertical jump
• Broad jump
• Bounding drills
• Pogo jumps
• Lateral hop and stick
• Reformer jumping
• Hurdles (forwards and lateral)
• Wall acceleration drills

5. Return to sport should be guided by clinical findings and is variable between different athletes. Generally, football players have shorter return to play timeframes than ballet due to the amount of time spend en pointe, jumping and landing. It may take 4-6 weeks to return to play in less irritable cases, and around 4 months for dancers to return to full performance⁸.
In athletes such as fast bowlers and soccer players, the posterior impingement test and previously provocative movements should be pain-free.
Lower limb strength and mobility asymmetries should have been addressed in the previous phases. There should be a gradual build up in training volume e.g. number of bowling deliveries, time spent on the soccer field, amount of jumping and landing in the dance studio.

Small studies have shown that conservative treatment alone has good prognostic outcomes, with up to two-thirds of cases resolving⁹.

When conservative management fails to relieve symptoms after 12 weeks, surgery is warranted. This may involve excising the problematic bony structures (e.g. os trigonum) and accessory muscles, or releasing hypertrophic scar tissue and the FHL tendon sheath. Special consideration should be considered with os trigonum excision as it is a weightbearing structure when the ankle is in full plantarflexion. Removal will result in greater pressure on the surface of the talus due to a reduction in surface area available for articulation. This can predispose athletes to subtalar joint osteoarthritis over time.

There has been a shift away from open surgery towards a less invasive endoscopic approach due to faster recovery times, and reduced complications¹⁰. Complications from surgery include infection, damage to the medial neurovascular bundle (using a posteromedial approach) and sural nerve (posterolateral approach). Surgery yields very good outcomes, with studies reporting success rates of around 80%¹¹. Return to play following endoscopic surgery is similar to conservative timeframes, however, most studies only looked at professional athletes.

Summary

PAI usually presents in athletes that repetitively load their ankle joint in plantarflexion. A number of structures at the back of the ankle can contribute to symptoms- these can be bony or soft tissues. The presence of os trigonum and FHL tenosynovitis are the most common features of PAI. Careful assessment is required to determine the cause of symptoms and differentiate PAI from other pathologies. Most cases of PAI can be managed conservatively with a period of offloading, anti-inflammatories, and targeted strengthening exercises. Surgery is warranted after unsuccessful conservative management and has favourable outcomes.

Julian Tubman (APAM)
Physiotherapist

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