Flexor Digitorum Longus Anatomy

Flexor digitorum longus (FDL) is the most medial of the three muscles of the deep posterior compartment. It arises from the posterior surface of the tibia below the soleal line, the only one of the three deep flexors to arise solely from the tibia, and its tendon runs behind the medial malleolus, crosses the sole and divides into four slips for the lateral four toes.

Why it matters to a surgeon. Two features dominate. The first is that FDL is relatively expendable: its tendinous interconnections with flexor hallucis longus at the knot of Henry mean that after harvest the lesser toes usually retain active flexion, driven onward by FHL through the interconnection. That underpins its role as the standard donor for FDL transfer in stage II posterior tibial tendon dysfunction, one of the highest-yield operations in foot and ankle surgery. Relatively is the load-bearing word, and the anatomy section below puts a number on it: the interconnection preserves movement rather than strength, and it is not guaranteed to be present in the foot in front of you.

The second is that FDL is a deforming force. Once the intrinsic muscles of the foot fail, in neuropathy, in cavovarus, after a compartment syndrome, in the diabetic foot, the unopposed long flexors and long extensors produce the claw toe, and FDL is the muscle pulling the interphalangeal joints into flexion.

Origin. The posterior surface of the tibia below the soleal line and medial to the vertical ridge, from just below the soleal line to within a few centimetres of the distal tibia, with some fibres from the fascia covering tibialis posterior. It is the only deep posterior compartment muscle arising solely from the tibia: tibialis posterior arises from tibia, fibula and interosseous membrane, and flexor hallucis longus principally from the fibula.

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Course at the ankle. The tendon forms in the distal third of the leg and crosses superficial (posterior) to the tibialis posterior tendon at about the level of the medial malleolus, so that in the tarsal tunnel FDL lies immediately posterior to tibialis posterior. It passes behind the malleolus in its own groove and synovial sheath beneath the flexor retinaculum, then turns forward beneath the sustentaculum tali, still superficial to tibialis posterior.

Course in the sole. It runs forward and laterally, crossing deep (dorsal) to flexor hallucis longus at the knot of Henry beneath the navicular and medial cuneiform, where the two tendons exchange slips. It receives the insertion of quadratus plantae (flexor accessorius) on its lateral border, divides into four tendons for the second to fifth toes, and gives origin to the four lumbricals: the first from the medial side of the second tendon (unipennate), the second to fourth from the adjacent sides of the tendons (bipennate).

Insertion. Each tendon passes through the split in the corresponding flexor digitorum brevis tendon, the same relationship as flexor digitorum profundus and superficialis in the hand, and inserts on the plantar base of the distal phalanx of the second to fifth toes. Brevis stops at the middle phalanx, so FDL is the only flexor of the distal interphalangeal joints of the lesser toes.

Innervation. The tibial nerve, root values S1 and S2, with an L5 contribution described in some sources. Motor branches arise in the proximal third of the leg and enter the deep surface of the muscle. The tibial nerve reaches the deep compartment beneath the tendinous soleal arch, so a lesion there denervates FDL along with tibialis posterior and flexor hallucis longus.

The lumbricals and quadratus plantae are supplied differently. Quadratus plantae takes the lateral plantar nerve (S2, S3). The first lumbrical takes the medial plantar nerve and the second to fourth the lateral plantar nerve, directly analogous to the hand. A lateral plantar nerve lesion therefore denervates quadratus plantae and three of the four lumbricals, removing the vector correction described below and unbalancing the toes, which contributes to lesser toe deviation and clawing. It is one of the mechanisms by which a tarsal tunnel syndrome or a distal tibial nerve lesion produces lesser toe deformity.

Root value logic. S1 is tested by plantarflexion, eversion and the ankle jerk; S2 contributes to toe flexion and the intrinsics. Weak lesser toe flexion with weak inversion localises to the tibial nerve or the deep posterior compartment. Weak lesser toe extension localises to L5 and the deep peroneal nerve, a different problem entirely.

Blood supply. Muscular branches of the posterior tibial artery, with a contribution from the peroneal artery proximally. The tendon is fed through a mesotendon and vincular system from the posterior tibial artery and distally from the medial and lateral plantar arteries. FDL is a well-vascularised, robust tendon, which is part of why it makes a good transfer donor, and it has no equivalent of the notorious watershed segment that afflicts the tibialis posterior tendon just distal to the medial malleolus. It is never used as a muscle flap: it is deep, functionally significant, and supplied by unnamed segmental branches, and deep posterior compartment muscle is not sacrificed for soft tissue cover.

Relations in the leg. FDL is the most medial of the deep posterior compartment muscles, lying on the posterior surface of the tibia. Tibialis posterior lies lateral and deep to it, flexor hallucis longus lateral on the fibula, and the deep transverse fascia and beyond it the soleus behind. The posterior tibial artery and tibial nerve lie on the posterior surface of tibialis posterior and FDL, between them and the deep transverse fascia.

At the ankle: the tarsal tunnel. Anterior to posterior beneath the flexor retinaculum the order is tibialis posterior, flexor digitorum longus, posterior tibial artery and veins, tibial nerve, flexor hallucis longus. FDL lies immediately posterior to tibialis posterior and immediately anterior to the neurovascular bundle, and that relationship defines the safe plane for harvest: between the two tendons and strictly anterior to the bundle. The tibial nerve divides into medial and lateral plantar nerves within or just distal to the tunnel, and the first branch of the lateral plantar nerve (Baxter nerve) arises here.

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In the sole. FDL runs deep to the plantar aponeurosis and flexor digitorum brevis (first layer), forming part of the second layer of the sole with FHL, quadratus plantae and the lumbricals. The lateral plantar nerve and artery run laterally across the sole between the first and second layers, immediately superficial to quadratus plantae. Distally each tendon passes through the split in the corresponding brevis tendon within the fibro-osseous flexor sheath of the toe.

Actions. The first is the one no other muscle can perform:

• Flexion of the distal interphalangeal joints of the second to fifth toes, its unique and irreplaceable action, since flexor digitorum brevis reaches only the middle phalanges
• Flexion of the proximal interphalangeal and metatarsophalangeal joints of the lesser toes, assisted by brevis and the intrinsics
• Plantarflexion of the ankle, weak, with a small moment arm
• Inversion of the hindfoot and dynamic support of the medial longitudinal arch, because it passes beneath the sustentaculum tali and along the medial column, synergistic with tibialis posterior

In gait. FDL is active from mid-stance to terminal stance, peaking around heel rise. It presses the toes to the floor during push-off, which broadens the weightbearing base of the forefoot, stabilises the toes against the ground and increases the effective lever arm of the foot. Toe purchase matters: a foot in which the toes do not touch the ground at push-off loads the metatarsal heads more heavily, which is one mechanism of metatarsalgia in a claw toe foot. FDL is in phase with tibialis posterior, which is why it can be transferred to substitute for it without any need for phase re-education.

Strength and excursion. These are the numbers that drive transfer surgery, and the comparison with tibialis posterior is the one an examiner wants:

When FDL fails. In isolation the loss is active distal interphalangeal flexion of the lesser toes, detectable on examination but rarely a functional complaint, and loss of toe purchase at push-off, which transfers load to the metatarsal heads. In combination with intrinsic failure the picture is very different: FDL becomes a deforming force, and clawing results.

Palpation. The tendon can be felt immediately posterior to the tibialis posterior tendon behind the medial malleolus, with the toes actively flexed and relaxed.

Isolating the long flexor. Stabilise the middle phalanx of a lesser toe and ask the patient to flex the distal interphalangeal joint. Flexor digitorum brevis inserts on the middle phalanx and cannot flex the DIP joint, so DIP flexion is FDL alone, directly analogous to isolating flexor digitorum profundus in the hand. Absent or weak DIP flexion means FDL laceration, rupture, denervation or a completed transfer, allowing for pain inhibition and a stiff DIP joint as false positives.

Isolating the short flexor. Hold all the other toes in extension, which tenodeses the common FDL muscle belly, and ask for PIP flexion of the tested toe.

Named tests and signs. The tests that matter around this tendon:

The vocabulary of lesser toe deformity. Examiners test it, and the joint positions are what separate the three:

• Claw toe: metatarsophalangeal joint extended, proximal interphalangeal flexed, distal interphalangeal flexed. Usually multiple toes, and usually neurological, from intrinsic failure with unopposed long flexors and extensors
• Hammer toe: metatarsophalangeal joint neutral or extended, proximal interphalangeal flexed, distal interphalangeal neutral or extended. Usually a single toe, often the second, and usually mechanical: footwear, a long second ray, or hallux valgus crowding
• Mallet toe: distal interphalangeal flexed alone, with the MTP and PIP normal. This is specifically an FDL problem, and it is the deformity most reliably corrected by a simple flexor tenotomy

Always look for the cause. Flexibility is settled by the push-up test in the table above. A claw toe pattern in multiple toes then demands a neurological examination: diabetes, Charcot-Marie-Tooth disease, a previous compartment syndrome, a spinal lesion. Treating the toes without diagnosing the neuropathy is a missed diagnosis.

Related pages. The tendon this one replaces: Tibialis Posterior Anatomy is the failing motor, and Flatfoot Deformity - Adult is the deformity the transfer is performed for, with Flexible Flatfoot and Rigid Flatfoot separating the feet that can be reconstructed from those that need fusion. Spring Ligament Insufficiency is the ligament failure a tendon transfer cannot hold against on its own.

FDL transfer for stage II posterior tibial tendon dysfunction is the operation this anatomy exists to serve, and the tabs below take it from indication to the structures that can be damaged.

Lesser toe deformity and flexor surgery. The intrinsic muscles, the interossei and lumbricals, flex the metatarsophalangeal joints and extend the interphalangeal joints. When they fail, in neuropathy, cavovarus or a previous compartment syndrome, the long extensors extend the MTP unopposed and the long flexors flex the interphalangeal joints unopposed, and the result is the claw toe.

The MTP joint is the key. Once the MTP hyperextends, the plantar plate is drawn distally, the metatarsal head is driven plantarwards, the fat pad migrates distally and no longer cushions the head, and metatarsalgia and plantar keratosis follow. Correcting the toe alone without addressing the MTP joint will not relieve the metatarsalgia.

A flexible deformity (positive push-up test) is treated with soft tissue:

• Flexor tenotomy: simple division of the flexor tendon, percutaneous or open
• Flexor-to-extensor transfer (Girdlestone-Taylor): the FDL tendon is split longitudinally and both limbs are passed dorsally either side of the proximal phalanx and sutured to the extensor hood, converting the deforming flexor into an MTP flexor and IP extensor and reproducing the lost intrinsic function. It requires a flexible deformity and is combined with an MTP release where the joint is contracted

A fixed deformity (negative push-up test) needs bone, and soft-tissue procedures alone will recur:

• PIP resection arthroplasty or arthrodesis for the interphalangeal component
• MTP release, extensor lengthening and a shortening metatarsal osteotomy (Weil) for the MTP component

Percutaneous flexor tenotomy in the diabetic foot. The indication is a neuropathic ulcer at the tip of a clawed or hammered toe in a patient with adequate perfusion. The deformity drives the tip of the distal phalanx into the ground, and no dressing or offloading device will heal an ulcer that is being re-traumatised at every step.

The procedure is a percutaneous division of the flexor tendon at the plantar aspect of the toe through a needle or a small blade stab incision, usually under local anaesthetic in the clinic, taking seconds per toe. The tendon lies immediately deep to the plantar skin at the level of the proximal or middle phalanx, with the digital neurovascular bundles at the plantar-medial and plantar-lateral corners, so aim strictly midline plantar and pass the blade transversely against the bone. The toe straightens, the tip lifts off the ground, and the ulcer offloads; reported healing rates are high and recurrence rates low, with a very low complication rate, which makes it a genuinely high-value, low-cost, low-risk intervention.

Prerequisites and counselling. Adequate arterial perfusion, no active spreading infection or osteomyelitis requiring other treatment, and a flexible deformity, since a rigidly fixed toe needs a bony procedure. The toe will float slightly and lose active flexion; in a neuropathic foot this is a trivial price for ulcer healing, and patients should be told it will happen.

Tenosynovitis of the FDL occurs alongside tibialis posterior tenosynovitis in the medial hindfoot, and can contribute to tarsal tunnel symptoms by crowding the tunnel.

Laceration of the FDL in the sole or behind the medial malleolus is uncommon and, in isolation, well tolerated. It should be looked for specifically in any medial ankle or plantar laceration, alongside the tibial nerve.

Flexor digitorum accessorius longus is an accessory muscle arising in the deep posterior compartment and inserting into the FDL or quadratus plantae. It is present in a minority of feet and is a recognised cause of tarsal tunnel syndrome by occupying space in the tunnel; it is also a recognised incidental MRI finding that should not be mistaken for a mass.

Deep posterior compartment syndrome infarcts FDL along with FHL and tibialis posterior. The late sequel is fixed clawing of the toes with plantar sensory loss and a cavovarus foot.

Other operations involving FDL. The tendon is met, moved or endangered in other operations too:

• Posteromedial approach to the tibia: the FDL is elevated from the posterior tibia, with the neurovascular bundle retracted, giving access to the posterior tibial cortex for plating a posterior malleolar fragment or grafting a nonunion
• Posteromedial fasciotomy: the incision lies 1 to 2 cm posterior to the posteromedial tibial border. The superficial posterior compartment is opened first, then the deep transverse fascia must be deliberately divided to release the deep compartment containing FDL. Failing to do so is the classic incomplete fasciotomy, and its late sequel is a clawed, insensate foot
• Tarsal tunnel release: the FDL sheath is opened as part of the release, and an accessory flexor digitorum accessorius longus is excised if present
• FDL transfer to the fifth metatarsal base: used to restore eversion when both peroneal tendons are irreparable
• FDL transfer for Achilles reconstruction: an alternative to FHL, weaker but preserving hallux function; occasionally preferred in a dancer or sprinter
• Calcaneal fracture fixation: a screw directed from lateral to medial into the sustentacular fragment can transfix the FDL and the neurovascular bundle if it over-penetrates the medial cortex

FDL as a donor. Flexor digitorum longus is the textbook example of a good transfer donor, and the reasons generalise to any tendon transfer:

1. Expendable: its function is duplicated or compensated, here by the FHL interconnection at the knot of Henry
2. Adequate excursion for the intended job
3. In phase with the recipient, so no re-education is needed
4. A straight line of pull through a smooth gliding bed, without an acute turn
5. Adequate power, though here the power is inadequate to substitute fully, which is why the transfer is combined with a bony procedure. That candid limitation is precisely the point examiners want acknowledged
6. A supple, passively correctable recipient joint: stage II, not stage III

Anatomical variation across populations

• Knot of Henry interconnections are consistently present but variable in pattern. The commonest arrangement transmits drive from FHL to FDL, but reciprocal slips and more complex patterns occur, and the slips vary in number and thickness. The functional consequence of a harvest therefore cannot be assumed to be identical in every foot, and the surgeon should inspect the interconnection directly.
• Quadratus plantae varies in the presence and size of its two heads; the lateral head is absent in a minority of feet, which theoretically alters the vector correction.
• Flexor digitorum accessorius longus is an accessory muscle present in a minority of feet, arising in the deep posterior compartment and inserting into the FDL or quadratus plantae. It is a recognised cause of tarsal tunnel syndrome and an incidental MRI finding that should not be mistaken for a mass.
• Lumbrical number and configuration occasionally varies, with absence of the fourth lumbrical described.

Side-by-side guidance

Resource-dependent practice

• Well-resourced settings: weightbearing CT, MRI, interference screw fixation, spring ligament internal bracing, arthroereisis implants.
• Limited-resource settings: the diagnosis of stage II posterior tibial tendon dysfunction is entirely clinical - too-many-toes, single heel raise, passive correctability - and weightbearing radiographs suffice for planning. The FDL transfer with medial displacement calcaneal osteotomy requires only a saw, two screws, suture and basic instruments, and is fully deliverable at district hospital level. A well-executed triple arthrodesis remains a reliable operation for a rigid deformity where implants are limited.
• Percutaneous flexor tenotomy is one of the highest-value interventions in global diabetic foot care: it requires a blade, local anaesthetic and a few minutes, and it converts a chronically non-healing tip ulcer into a healing one. In settings where amputation is the default endpoint for a chronic toe ulcer, its availability changes outcomes substantially.

Registry and outcome signals

• There is no dedicated registry for flatfoot reconstruction or lesser toe surgery. Institutional cohorts consistently show durable improvement after combined FDL transfer and bony realignment for flexible stage II deformity, with the main causes of failure being under-correction, an unaddressed gastrocnemius contracture, and unrecognised fixed forefoot varus.
• Diabetic foot series consistently report high ulcer healing rates and low recurrence at the treated toe after percutaneous flexor tenotomy, with the principal caveats being adequate perfusion and a flexible deformity.
• Major trauma and open fracture audits consistently link delayed or incomplete fasciotomy - most often failure to release the deep posterior compartment - to poor functional outcomes including fixed toe clawing.