Ankle and Foot

Part 3 · The lower limb

The ankle mortise, its ligaments, and the arches of the foot

The impossible brief

Figure 1 · One foot, two jobs

The foot has to be two different things within the same stride, roughly half a second apart:

• At heel strike and early stance, it must be a mobile, compliant shock absorber, unlocking to accommodate uneven ground and to dissipate an impact of two to three times body weight.
• At push-off, it must be a rigid lever, stiff enough to transmit the entire propulsive force of the calf without collapsing.

The mechanism that switches between the two is the coupling of subtalar pronation and supination with midtarsal joint mobility — and understanding that mechanism is the single most useful thing in this chapter. Almost every foot condition you will treat is a failure of it.

Over a lifetime the foot performs this transformation something like 150 million times. That repetition, in a structure of 26 bones, 33 joints and only 2 mm of skin between bone and ground, is why the foot carries the highest overuse pathology burden in the body.

Learning outcomes

• Describe the ankle (talocrural) joint: surfaces, mortise, ligaments, movements and stability.
• Describe the syndesmosis and explain high ankle sprain.
• Describe the subtalar and midtarsal joints and explain triplanar motion.
• Explain the windlass mechanism and the mobile-adapter to rigid-lever transformation.
• Describe the arches and their passive and dynamic supports.
• Describe the retinacula, tendon sheaths and the tarsal tunnel.
• Name the intrinsic muscles of the foot in four layers and state their nerve supply.
• Describe the nerve and blood supply of the foot and their clinical assessment.
• Describe the phases of the gait cycle and what the foot does in each.
• Explain lateral ankle sprain, syndesmotic injury, plantar fasciopathy, tibialis posterior dysfunction, hallux valgus and the diabetic foot, with their rehabilitation implications.

The ankle (talocrural) joint

Figure 2 · Bones of the foot

Figure 3 · The ankle mortise and its ligaments

Surfaces and the mortise

A synovial hinge joint with one degree of freedom (though with a slightly oblique axis, so its motion is not purely sagittal).

• The mortise is formed by the tibial plafond above, the medial malleolus medially, and the lateral malleolus laterally. It is a bony bracket, and it is the reason the ankle is far more stable than the wrist.
• The talar trochlea is wider anteriorly than posteriorly — by around 5 mm.

The consequence of that wedge shape is the single most examinable fact about the ankle:

Hence the classic inversion sprain occurs in plantarflexion and inversion, and hence full dorsiflexion is the safest position to test and to weight-bear in.

Resting position: ~10° plantarflexion, midway between inversion and eversion. Capsular pattern: plantarflexion more limited than dorsiflexion.

Ligaments

Movements

The talocrural axis runs obliquely, from just below the medial malleolus to just below the lateral malleolus — angled about 8° from the frontal plane and 20–30° externally rotated in the transverse plane. Because it is oblique, dorsiflexion is accompanied by slight abduction and eversion, and plantarflexion by adduction and inversion. This is why “pure” sagittal ankle motion does not exist.

The Silfverskiöld test distinguishes gastrocnemius from soleus restriction: measure dorsiflexion with the knee extended (loading the biarticular gastrocnemius) and then flexed (unloading it). More dorsiflexion with the knee flexed implicates gastrocnemius.

The subtalar and midtarsal joints — the transformation mechanism

Subtalar (talocalcaneal) joint

The articulation between talus and calcaneus, in anterior, middle and posterior facets, with the sinus tarsi and the interosseous talocalcaneal ligament between the middle and posterior facets.

Its axis is oblique in all three planes — running approximately 42° from the horizontal and 16° from the sagittal — which means every motion at this joint is triplanar:

In closed chain (weight bearing), the same joint motions appear differently because the calcaneus is fixed to the ground: pronation appears as calcaneal eversion with talar adduction and plantarflexion, and therefore obligatory internal rotation of the tibia and femur. Supination produces the reverse.

This coupling is the mechanical link between the foot and the rest of the limb. Excessive or prolonged pronation drives tibial internal rotation, which drives femoral internal rotation and dynamic knee valgus — the pathway connecting foot mechanics to patellofemoral pain, ITB syndrome and ACL risk. It is also why foot orthoses can influence proximal symptoms and why hip strength can influence foot symptoms.

Midtarsal (transverse tarsal, Chopart’s) joint

Talonavicular + calcaneocuboid, forming an S-shaped line across the foot — the surgical amputation level of the same name.

Its behaviour is the key to the transformation:

• When the subtalar joint is pronated, the axes of the talonavicular and calcaneocuboid joints become parallel, the midtarsal joint is unlocked, and the foot is a mobile, compliant adapter.
• When the subtalar joint is supinated, the two axes diverge, the midtarsal joint locks, and the foot becomes a rigid lever.

That is the mechanism the whole chapter turns on. Heel strike → subtalar pronation → midtarsal unlocked → shock absorption and terrain accommodation. Midstance to toe-off → subtalar supination → midtarsal locked → rigid lever for propulsion.

The windlass mechanism

Described by Hicks. The plantar aponeurosis runs from the calcaneal tuberosity to the plantar plates and bases of the proximal phalanges, passing beneath the metatarsal heads.

During toe-off, the MTP joints extend (dorsiflex). The aponeurosis wraps around the metatarsal heads like a cable around a drum, shortening the distance between the calcaneus and the metatarsal heads. This:

• Raises and stiffens the medial longitudinal arch
• Supinates the hindfoot, which locks the midtarsal joint
• Converts the foot into a rigid lever, entirely passively

It is an elegant purely mechanical solution, requiring no muscular effort, and it is testable at the bedside: passively extend the hallux in a standing patient and watch the arch rise (a positive Jack’s test). Failure of the windlass — from hallux rigidus, plantar fascia rupture, or an incompetent first ray — is a common and under-diagnosed cause of forefoot and arch pain.

The arches and their support

Figure 4 · The arches and the windlass

The hierarchy of support — the order matters and is a standard examination point:

• Bone shape (the wedge-shaped cuneiforms and the arch’s own geometry)
• Ligaments — especially the spring ligament and the plantar aponeurosis, which contributes an estimated 25% of arch stiffness
• Muscles — which contribute little in quiet standing but progressively more with load, fatigue and propulsion

This explains why arch collapse follows ligament failure (spring ligament attenuation) or tendon failure (tibialis posterior dysfunction) rather than simple “weak muscles”, and why intrinsic foot muscle training, though useful, is not a complete answer to a collapsing arch.

Pes planus (flatfoot) must be classified before it is treated: flexible (arch present on tiptoe or with Jack’s test — usually asymptomatic and normal in children under 5–6) versus rigid (no arch reformation — consider tarsal coalition, particularly in an adolescent with a stiff, painful flatfoot and recurrent “ankle sprains”). Pes cavus (high arch) should prompt a neurological review — bilateral cavovarus feet with clawed toes suggest Charcot–Marie–Tooth disease until proved otherwise.

Retinacula, sheaths and tunnels

The tarsal tunnel

Contents, from anterior to posterior — “Tom, Dick And Very Nervous Harry”:

Tibialis posterior · Flexor Digitorum longus · Artery (posterior tibial) · Vein · Nerve (tibial) · Flexor Hallucis longus

Tarsal tunnel syndrome produces burning, tingling and aching in the sole, worse on standing and walking, with a positive Tinel’s sign behind the medial malleolus. Causes include space-occupying lesions (ganglion, varicosities), post-traumatic fibrosis, and hindfoot valgus stretching the nerve. It is often confused with plantar fasciopathy, and the distinguishing features are the burning quality, the nocturnal component, and the sensory rather than mechanical pattern.

Note the FHL groove beneath the sustentaculum tali: FHL tenosynovitis here is a classic dancer’s injury, often with posterior ankle impingement from an os trigonum.

The intrinsic muscles

Dorsum: extensor digitorum brevis and extensor hallucis brevis — the only intrinsic muscles supplied by the deep fibular nerve. A visible fleshy mass over the lateral dorsum is normal EDB, frequently mistaken for swelling.

Sole — four layers, all supplied by the medial and lateral plantar nerves (tibial):

The nerve supply rule: the medial plantar nerve supplies only four muscles — abductor hallucis, flexor digitorum brevis, flexor hallucis brevis and the first lumbrical (the exact foot equivalent of the median nerve’s LOAF in the hand). The lateral plantar nerve supplies everything else, exactly as the ulnar nerve does in the hand.

Reference axis: in the foot, abduction and adduction are defined relative to the second toe (compare the middle finger in the hand).

Quadratus plantae is a foot-specific muscle with no hand equivalent: it corrects the oblique line of pull of the FDL tendons, which enter the sole obliquely from the medial side, so that the toes flex straight rather than deviating medially.

Functionally, the intrinsics behave as the foot’s “local stabilisers” — active mainly in the second half of stance, stiffening the arch, controlling toe position, and contributing to balance. They atrophy with prolonged shoe use and immobility, and short-foot and toe-yoga exercises have reasonable evidence for improving arch control and balance, though not for changing static arch height.

Nerves and vessels of the foot

Cutaneous supply — the map

Arteries

• Dorsalis pedis — the continuation of the anterior tibial artery, palpable lateral to the EHL tendon on the dorsum. Absent or non-palpable in up to 10% of normal people, so its absence alone is not diagnostic.
• Posterior tibial artery — palpable behind the medial malleolus, midway between it and the Achilles tendon; divides into the medial and lateral plantar arteries, which with the deep plantar branch of dorsalis pedis form the plantar arch.

Assessment:

• palpate both pulses in every foot presentation, and measure the ankle–brachial pressure index (ABPI) where there is any suspicion of arterial disease. Normal is 0.9–1.3
• below 0.9 indicates peripheral arterial disease
• above 1.3 suggests incompressible, calcified vessels — common in diabetes and a falsely reassuring result. Compression therapy for oedema is contraindicated below an ABPI of about 0.8 without specialist input

The gait cycle, in foot terms

Stance is ~60% and swing ~40% of the cycle, with two periods of double support totalling ~20% — which disappear in running, the defining difference between the two.

Common gait deviations and their anatomical cause:

Clinical conditions

Lateral ankle sprain

The commonest musculoskeletal injury in sport, and the one most often dismissed.

• Mechanism: inversion with plantarflexion — the loose-packed position.
• Order of injury: ATFL → CFL → PTFL.
• Grading: I (stretch, minimal laxity), II (partial tear, moderate laxity), III (complete rupture, marked laxity).
• Tests: anterior drawer (ATFL), talar tilt (CFL). Apply the Ottawa ankle rules to decide on radiography: pain in the malleolar or midfoot zone plus bone tenderness at the posterior edge or tip of either malleolus, the navicular, or the base of the fifth metatarsal, or inability to weight-bear four steps immediately and in the department.
• Do not miss: the proximal fibula (Maisonneuve), the base of the fifth metatarsal, syndesmotic injury, osteochondral lesions of the talus, and, in adolescents, a distal fibular physeal (Salter–Harris I) injury where the physis is tender rather than the ligament.
• The under-appreciated problem is what happens next. Up to 40% of ankle sprains develop chronic ankle instability, with persistent giving way, recurrent sprain and reduced function, driven as much by proprioceptive deficit and altered neuromuscular control as by mechanical laxity. Balance and proprioceptive training reduces recurrence substantially and is not optional. Early functional rehabilitation with weight bearing outperforms immobilisation.

Syndesmotic (“high ankle”) sprain

• Mechanism: external rotation with dorsiflexion, forcing the talus to splay the mortise.
• Presentation: pain above the joint line over the AITFL, pain on the squeeze test and external rotation stress test, and pain on single-leg hop.
• Prognosis: recovery takes roughly twice as long as a lateral sprain, and unstable injuries require surgical stabilisation. Always palpate the proximal fibula — a Maisonneuve fracture will otherwise be missed.

Plantar fasciopathy

The commonest cause of plantar heel pain.

• Presentation: sharp pain under the medial calcaneal tubercle, worst with the first steps in the morning and after periods of rest, easing with movement and returning after prolonged loading.
• Pathology: degenerative (fasciopathy, not fasciitis) — collagen disorganisation and angiofibroblastic change, as in tendinopathy (Chapter 7).
• Note on the heel spur: present in a large proportion of asymptomatic people and not the cause of the pain. Explaining this is often therapeutic in itself.
• Management: load management, calf and plantar fascia stretching, and high-load plantar fascia–specific strength training (heel raises with the toes extended over a towel, to engage the windlass) which has good trial evidence; taping and orthoses for short-term relief; addressing body mass and training error. Corticosteroid injection gives short-term relief with a risk of fat pad atrophy and fascial rupture.
• Differentials: fat pad atrophy (pain more central and diffuse), calcaneal stress fracture (positive squeeze test, night pain), tarsal tunnel or Baxter’s nerve entrapment (burning, sensory symptoms), and S1 radiculopathy.

Tibialis posterior tendon dysfunction (adult acquired flatfoot)

The commonest cause of progressive adult flatfoot, typically in women over 40, and frequently missed until deformity is fixed.

The single-leg heel raise is the key test — an inability to perform one, or to invert the heel while doing it, is the earliest reliable sign. Stages I and II are the physiotherapy window: orthoses, eccentric and concentric tibialis posterior strengthening (which has good trial evidence), and activity modification. Once rigid, it is surgical.

Forefoot conditions

The diabetic foot — a mandatory competence

Peripheral neuropathy (loss of protective sensation), peripheral arterial disease, and impaired healing combine to make the diabetic foot the leading non-traumatic cause of lower-limb amputation.

The rules that matter:

• Screen every diabetic foot: 10 g monofilament at defined sites, vibration sense, pulses and ABPI, skin condition, deformity, footwear.
• Loss of protective sensation means the patient cannot warn you. No thermal modalities, no hot packs, no unmonitored heat, and no aggressive tissue techniques over insensate skin (Chapter 8).
• Ulcers occur where pressure concentrates — the metatarsal heads, the hallux, and the heel. Offloading is the treatment; total-contact casting is the gold standard for a plantar neuropathic ulcer.
• Charcot neuroarthropathy is the emergency to recognise: a hot, red, swollen foot in a neuropathic patient, often with minimal pain and no evidence of infection, with a temperature difference of >2°C compared to the other foot. Radiographs may be normal early. It is routinely misdiagnosed as cellulitis, gout or a sprain, and continued weight bearing destroys the midfoot within weeks. Immediate immobilisation and offloading, and urgent specialist referral, are the response.
• Exercise remains indicated in diabetes — weight-bearing exercise is not contraindicated in the absence of active ulceration, and the older blanket advice to avoid it has been revised.

Where students consistently go wrong

• Confusing inversion/eversion with supination/pronation. Inversion and eversion are the frontal-plane components; supination and pronation are the triplanar composites.
• Forgetting the talar wedge. Dorsiflexion is close-packed; plantarflexion is vulnerable.
• Getting the lateral ligament order wrong. ATFL → CFL → PTFL.
• Treating an ankle sprain as trivial. Up to 40% develop chronic instability without proprioceptive rehabilitation.
• Not palpating the proximal fibula in an ankle injury. Maisonneuve.
• Calling plantar heel pain “fasciitis” and blaming the spur. Neither is accurate.
• Missing tibialis posterior dysfunction in stage I or II, when it is treatable.
• Forgetting the windlass. Hallux rigidus and hallux valgus destroy it, and that is why forefoot pain follows.
• Applying heat or vigorous technique to an insensate diabetic foot.
• Mistaking Charcot neuroarthropathy for infection or a sprain.

Check yourself

15 questions on this chapter. Tap one to see the answer and the reasoning.

Quick review

Further reading

Chapter 16 of 24 · Human Anatomy · Physiotherapist India End of Part 3 — The lower limb. Next: Chapter 17 — Vertebral Column and Back, opening Part 4.

Reviewed by the Physiotherapist India Team. · Human Anatomy contents