Peroneal spastic flatfoot is a condition that, despite its name, is often misunderstood. Historically used to describe a painful and rigid flatfoot deformity accompanied by a tight, spastic peroneal muscle, the term actually encompasses a variety of underlying pathologies. While the “spasm” of the peroneal muscles is the most visible sign, it is usually a secondary reaction to an underlying osseous or articular problem. This essay will explore the etiology, clinical presentation, diagnostic challenges, and evolving treatment landscape of peroneal spastic flatfoot, drawing on seminal research and recent clinical advancements.
The foundation for the modern understanding of this condition was laid by the groundbreaking work of Harris and Beath in 1948. They argued that the term “peroneal spastic flatfoot” was a misnomer, loosely and often inaccurately applied to rigid valgus feet arising from widely different causes . Their seminal study identified that the most common causes were not true muscle spasms, but two specific congenital anomalies of the tarsal bones: the calcaneonavicular bar and the talocalcaneal bridge . In these cases, the deformity is a fixed structural one due to this anomalous bony connection. The apparent spasm of the peroneal muscles is, in reality, an adaptive shortening, as the tarsal coalition restricts subtalar motion . Harris and Beath proposed that a more accurate term for such patients would be “rigid flat foot due to talocalcaneal bridge or calcaneonavicular bar” . They also identified a smaller group of patients, primarily those with inflammatory arthropathies like rheumatoid arthritis, who truly developed a valgus deformity from reflexive peroneal muscle spasm secondary to joint inflammation .
While tarsal coalitions remain a primary cause of rigid, “spastic” flatfoot , recent literature has identified another significant osseous etiology: the accessory anterolateral talar facet (AALTF) . This anatomical variant, present in a notable percentage of the population, can become a source of painful impingement . Research has shown that in some adolescents with peroneal spastic flatfoot, an AALTF causes lateral impingement between the talus and calcaneus at the sinus tarsi, leading to bone marrow edema and a subsequent protective peroneal muscle contracture . This condition, sometimes referred to as AALTF impingement (AATFI), creates a vicious cycle where the flatfoot deformity leads to impingement, which in turn causes pain and spasm, further rigidifying the foot . This understanding shifts the focus from a primary muscle problem to a bony impingement syndrome in a structurally malaligned foot .
Clinically, a patient with peroneal spastic flatfoot typically presents with a painful, rigid flatfoot deformity. The foot is held in pronation and abduction, and attempts to passively correct it are painful and unsuccessful . Pain is often localized to the lateral side of the foot, particularly in the region of the sinus tarsi . Diagnosis begins with a thorough physical examination, including gait analysis and assessment of foot alignment and range of motion . While standard weight-bearing radiographs may show signs like lipping of the talonavicular joint, which suggests an underlying anomaly, they often fail to directly visualize coalitions or the AALTF . Therefore, advanced imaging is crucial. CT and MRI scans are essential for confirming the diagnosis, ruling out other pathologies, and visualizing the exact nature of the bony abnormality, such as a fibrous coalition or the presence of an AALTF with associated bone marrow edema .
Treatment strategies have evolved from the foundational work of Harris and Beath, who first categorized the causes, to more nuanced and cause-specific interventions. Conservative management is often the first line of treatment. This can include rest, orthotics, physical therapy for stretching, and non-steroidal anti-inflammatory drugs . In cases where an AALTF and sinus tarsi syndrome are suspected, a diagnostic and therapeutic injection of a local anesthetic into the sinus tarsi can be used . A recent case report highlighted the success of a non-invasive approach: serial casting. By applying a below-knee cast with the foot in full plantar flexion and inversion, the authors were able to gradually stretch the peroneal muscles and resolve the “spasm” in a young girl, suggesting that this method may work by normalizing proprioceptive input from the sinus tarsi .
When conservative measures fail, surgical intervention is considered, and the approach is dictated by the specific etiology. For symptomatic tarsal coalitions, the standard of care is surgical resection of the coalition, which can restore subtalar motion and relieve pain . In cases of rigid flatfoot caused by an AALTF, newer techniques are being explored. A 2025 case report detailed the successful use of subtalar arthroereisis in an 11-year-old boy with AATFI . This minimally invasive procedure involves placing an implant in the sinus tarsi to limit excessive subtalar eversion, thereby correcting the flatfoot deformity and preventing the impingement that triggers the peroneal spasm . For more complex deformities, especially those involving structural malalignment, a combination of procedures may be necessary, including facet excision, peroneal tendon lengthening, and calcaneal osteotomy to correct the underlying flatfoot .
Peroneal spastic flatfoot is not a single disease but a clinical presentation with a spectrum of underlying causes, primarily congenital osseous anomalies like tarsal coalitions and the more recently recognized accessory anterolateral talar facet. The journey from Harris and Beath’s pivotal 1948 paper to modern surgical techniques illustrates a crucial evolution in orthopedic thought: moving from a descriptive, symptom-based label to a cause-driven, pathoanatomical understanding. This shift is vital because effective treatment—whether it be conservative casting, coalition resection, or subtalar arthroereisis—depends entirely on accurately identifying the root cause of the rigidity and pain. The future of managing this condition lies in continued refinement of diagnostic imaging and the development of minimally invasive, cause-specific surgical solutions that address the primary driver of the deformity and its secondary effects.