Peroneal spastic flatfoot is a clinical syndrome characterised by a painful, rigid flatfoot deformity accompanied by spasm of the peroneal muscles — most notably the peroneus longus and peroneus brevis. Unlike the common flexible flatfoot, which is generally benign and frequently asymptomatic, peroneal spastic flatfoot signals an underlying structural or pathological process that demands careful clinical evaluation. The condition is seen most frequently in adolescents and young adults, though it can occur at any age, and its recognition is essential because misdiagnosis or delayed treatment may lead to progressive joint damage and long-term disability.
Anatomy and Pathophysiology
To understand peroneal spastic flatfoot, it is necessary first to appreciate the anatomy of the subtalar joint and its relationship to the peroneal tendons. The subtalar joint, formed between the talus and calcaneus, governs the motion of inversion and eversion of the hindfoot. When this joint is irritated, restricted, or structurally abnormal, the peroneal muscles — which evert the foot and pass posterior to the lateral malleolus — reflexively contract in an attempt to splint and protect the joint. This guarding mechanism produces the characteristic peroneal spasm that gives the condition its name.
The spasm itself results in the foot being held in a position of eversion and abduction, creating the appearance of a flatfoot. Unlike flexible flatfoot, however, the arch does not reconstitute on tip-toe standing, and passive correction of the deformity is resisted and painful. Over time, if the underlying cause is not addressed, the sustained abnormal positioning can lead to adaptive contractures, further limiting subtalar and ankle motion.
Causes and Aetiology
The most well-recognised cause of peroneal spastic flatfoot is tarsal coalition — an abnormal bony, cartilaginous, or fibrous union between two or more tarsal bones. Calcaneonavicular and talocalcaneal coalitions are the most common types implicated in this condition. Tarsal coalitions are congenital in origin but often become symptomatic during adolescence, when ossification of the coalition increases rigidity and pain. The stiffened subtalar complex triggers peroneal spasm as a protective response.
Beyond tarsal coalition, peroneal spastic flatfoot may arise from a diverse range of other causes. Inflammatory arthritis, including juvenile idiopathic arthritis and rheumatoid arthritis, can irritate the subtalar joint sufficiently to provoke peroneal spasm. Osteochondral lesions of the talus — whether traumatic or avascular in origin — are another recognised cause, as are subtalar joint infections, os trigonum syndrome, and intra-articular loose bodies. Rare causes include tumours in and around the tarsal bones, such as osteoid osteoma, which may produce profound and disproportionate spasm. In some cases, no structural cause can be identified, and the spasm may be related to inflammatory synovitis alone.
Clinical Presentation
Patients with peroneal spastic flatfoot typically present with hindfoot pain and stiffness, often insidious in onset but occasionally precipitated by minor trauma or increased physical activity. The pain is usually localised to the sinus tarsi region, the peroneal tendons, or the subtalar joint itself. Walking on uneven ground is particularly provocative, as is prolonged standing.
On examination, the hindfoot is held in valgus (eversion), and the medial longitudinal arch is reduced or absent. Critically, this deformity is rigid — it does not correct with standing on tiptoes, distinguishing it clearly from flexible flatfoot. Passive inversion of the subtalar joint is restricted and painful, and any attempt to correct the foot position may trigger visible or palpable peroneal spasm. In longstanding cases, there may be associated ankle stiffness due to adaptive changes in the surrounding soft tissues.
Neurological examination is typically normal, distinguishing peroneal spastic flatfoot from conditions such as spastic diplegia or peroneal nerve palsy, which may superficially resemble the presentation. Gait analysis often reveals an antalgic pattern with reduced push-off on the affected side.
Investigations
Imaging is central to establishing the cause of peroneal spastic flatfoot. Plain radiographs of the foot and ankle, taken in weight-bearing positions, are the first-line investigation. Specific views such as the oblique projection are useful for identifying calcaneonavicular coalition, which appears as a bony bar between the anterior calcaneus and navicular. Talocalcaneal coalition, however, is more difficult to visualise on plain films and may only be suggested by secondary signs such as the “C-sign” on lateral views — a continuous C-shaped line formed by the medial outline of the talar dome and the posterior subtalar joint.
Computed tomography (CT) scanning has traditionally been the gold standard for confirming tarsal coalition, offering superior depiction of bony anatomy. Magnetic resonance imaging (MRI) is increasingly favoured, particularly when fibrocartilaginous coalition, bone oedema, osteochondral pathology, or soft tissue causes are suspected. MRI also avoids ionising radiation, an important consideration in the predominantly young patient population. In selected cases, nuclear bone scintigraphy may help localise areas of increased metabolic activity when other investigations are inconclusive.
Treatment
Management of peroneal spastic flatfoot is directed primarily at the underlying cause. In the acute phase, regardless of aetiology, conservative measures are employed to reduce pain and spasm. These include activity modification, non-steroidal anti-inflammatory medications, physiotherapy, and immobilisation in a below-knee cast or walking boot. In some patients, a short period of cast immobilisation is remarkably effective in breaking the spasm cycle and restoring a degree of subtalar mobility. Intra-articular corticosteroid injections may provide useful short-term relief where inflammatory synovitis is prominent.
When tarsal coalition is identified as the cause and conservative measures have failed, surgical intervention is considered. For calcaneonavicular coalition, resection of the bony bar with interposition of the extensor digitorum brevis muscle to prevent recurrence has well-established outcomes, particularly in younger patients with preserved subtalar motion. Talocalcaneal coalition resection is technically more demanding, and outcomes are less predictable, especially when the coalition involves more than fifty percent of the posterior subtalar facet — a threshold beyond which subtalar arthrodesis may be preferable.
In cases where significant joint damage or degenerative change has occurred, subtalar or triple arthrodesis (fusion of the subtalar, talonavicular, and calcaneocuboid joints) may be necessary to provide durable pain relief. While fusion sacrifices motion, it reliably eliminates pain and corrects deformity, allowing a return to functional activity.
Prognosis and Conclusion
The prognosis of peroneal spastic flatfoot depends heavily on early recognition and accurate identification of the underlying cause. When treated appropriately and in a timely fashion, the majority of patients achieve satisfactory pain relief and functional improvement. Delayed diagnosis, conversely, risks progressive joint deterioration, making surgical reconstruction more complex and outcomes less certain.
Peroneal spastic flatfoot is not a diagnosis in itself but a clinical sign that demands investigation. Its significance lies not in the flatfoot or the spasm, but in what those findings represent — a signal that the subtalar joint and surrounding structures are under stress. For the clinician, the imperative is to look beyond the surface presentation, identify the root cause, and institute appropriate management before irreversible damage occurs. With careful assessment and a thorough understanding of the condition’s diverse aetiology, excellent outcomes are achievable for the vast majority of affected patients.