Anatomical variations are body structures with morphological features differing from those described by the majority of anatomy literature [1]. They are commonly encountered in dissection sessions and clinical practice where 21% of experienced clinicians frequently report seeing variations, including the musculoskeletal system [1]. Accessory muscles and variations in the upper and lower extremities are often asymptomatic and therefore overlooked [2]. However, these musculoskeletal variations may become symptomatic leading to non-inflammatory problems, tissue masses, and exercise-related pain [2].
Superficial posterior crural muscles of the lower leg include the gastrocnemius, plantaris, and soleus. The soleus is a broad muscle which originates via tendinous fibers from the posterior fibular head, proximal third of the posterior surface of the fibular body, popliteal line, and middle third of the tibial medial border; inserts on the middle part of the posterior calcaneal surface by joining the gastrocnemius muscle to form the calcaneal tendon; blood supply is the posterior tibial artery, fibular (peroneal) artery, and sural arteries; innervation is the first and second sacral nerves via the tibial nerve; and functional action is ankle plantarflexion [3].
In comparison to the soleus, the accessory soleus muscle (ASM) varies in its origin and insertion. Origin attachment sites include the posterior aspect of the tibia, which is most like that of the soleus, and the deep aponeurosis of the soleus muscle [2]. There are five reported ASM insertion attachment sites including: (1) Achilles tendon; (2) superior calcaneus surface via fleshy muscular insertion; (3) superior calcaneus via tendinous insertion; (4) medial calcaneus via fleshy muscular insertion; and (5) medial calcaneus via tendinous insertion [2]. ASM blood supply is the posterior tibial artery, innervation is the first and second sacral nerves via the tibial nerve, and functional action is undocumented [4].
ASM is an anatomical variation found in approximately 10% of individuals [5]. ASM can be asymptomatic or symptomatic and can be involved in painful syndromes, particularly during physical activities or exercise [5]. The incidence of ASM ranges from 0.7% - 5.5% in cadaver studies and is present in anatomy texts dating back to the nineteenth century [6]. The first clinical cases of ASM were reported in 1965 by Dunn [6], who described two patients with muscles mimicking soft tissue tumors. Approximately 85% of documented cases occur unilaterally and are more common in males [7].
Invasive procedures such as surgical exploration and biopsy are the gold standard ASM diagnostic methods [6]. However, non-invasive procedures including plain magnetic resonance imagines (MRI), computerized tomography (CT), radiographs, or ultrasound (US) imaging are commonly performed [5]. With CT and US, ASM can be mistakenly identified as a soft tissue tumor, thus MRI is the preferred non-invasive diagnostic technique [5-6]. Furthermore, ASM has been described as being evaluated and treated with biopsy, fasciotomy, or excision [6].
The purposes of this paper were to describe an ASM cadaver specimen, review the literature regarding ASM, identify potential clinical implications in patient management, and develop a clinical decision making flowchart.
A cadaver specimen with ASM was identified during a graduate level dissection-based anatomy course (Figure 1). This finding prompted further review of the literature to determine whether the identified ASM agreed with prior documented cases and a clinical decision making flowchart (Figure 2) for symptomatic ASM was developed.
Carrington et al. [7] described a young, athletic patient who had ASM surgically removed due to exertional compartment syndrome and Tarsal Tunnel Syndrome (TTS). Surgical excision was performed in this symptomatic case and the patient reported relief of all symptoms after post-surgical recovery.
Bistaraki et al. [8] conducted a literature review of ASM but were unable to determine why some patients are symptomatic and others are not. The authors recommended further research to establish clinical protocols to identify ASM during the patient examination and guide treatment planning.
Christodoulou et al. [9] described a 17 year-old basketball player presenting with a soft tissue mass in his posteromedial left ankle that was diagnosed as an ASM. The patient reported that his pain gradually increased during running or jumping. Ultimately, the patient’s ASM was surgically excised, and the patient was able to return to full activities within eight weeks without any symptoms. The authors also conducted a literature review and described ASM as a bulging soft tissue mass posteromedial to the ankle with clinical symptoms including exertional pain. The authors noted that most cases of ASM are asymptomatic, so pain may not be exhibited. In addition, ASM is often identified in the late teenage years because of increased physical activity and muscle hypertrophy. Finally, ASM tends to be misdiagnosed as a ganglion, lipoma, hemangioma, synovioma, sarcoma, tumor, or inflammatory lesion.
Bojinca et al. [10] described a young male with moderate pain and swelling in the posteromedial aspect of his right ankle after exercise. The presence of ASM was confirmed using musculoskeletal ultrasonography. Based on this finding, a conservative physical therapy management approach was implemented with good results. The authors reported that ASM is commonly diagnosed as either a hemangioma or sarcoma because it is difficult to differentiate from a soft tissue tumor based on physical examination alone [10]. The most common symptom reported by people with ASM is ankle pain or discomfort during exertional activities or post-activity and associated with swelling of the ankle. ASM can cause compartment syndrome due to extrinsic compression of the tibial nerve during exercise [10]. Ischemic pain during exercise can also occur because ASM receives its arterial supply from the posterior tibial artery. The authors concluded that ASM should be considered by clinicians when diagnosing ankle pain and swelling in young athletes.
Luck et al. [11] conducted a retrospective case series study of electronic radiology records for cases with MRI-diagnosed ASM. Their findings suggest a strong association between ASM and calcaneal tendinopathy. The study included 13 cases of ASM, 9 of which also presented with calcaneal tendinopathy. The MRI examination indications included ankle pain, suspected calcaneal tendon disorders, palpable mass, suspected blood clot, and resection of squamous cell carcinoma. The study also highlighted potential clinical presentations of ASM, such as a painful mass at the posteromedial ankle that typically worsens with physical activity. Presentation of ASM often occurs during late adolescence due to muscle growth and increased activity with an approximate 2:1 male predominance. Additionally, the authors reported that ASM diagnosis should be considered in patients with a palpable mass in the posterior ankle or in those with a soft tissue density in Kager’s triangle (pre-calcaneal fat pad). Lastly, US, CT, and MRI can be used to identify the mass between the soleus and the flexor hallucis longus with MRI emphasized as the ideal method.
Doda et al. [12] described a 21 year-old male soldier with chronic ankle pain. Initially, the patient suffered an ankle sprain with pain that persisted for 2 months. This was followed by one-year of intermittent pain in the same ankle that worsened with running and jumping. Upon examination, the patient had tenderness around the tibialis posterior tendon and anterior talofibular ligament, however, no swelling or limitations in ankle range of motion were observed. A radiograph showed normal bone structure with an area of soft tissue density in the pre-calcaneal fat pad. An MRI determined the presence of ASM with increased intrafascial fluid and perimuscular edema. Treatment included six weeks in an ankle cast and non-steroidal anti-inflammatory drugs followed by physical therapy and discontinuation of running and jumping. After four months of treatment, a follow up MRI revealed resolution of the intrafascial fluid collection and edema around the ASM. The patient reported pain reduction and was able to return to his routine duties with the exception of heavy forms of exercise defined as jumping and running.
Gentile et al. [13] described an athletic, 39 year-old male’s five-year history of persistent left ankle pain. The patient was treated by several specialists and originally diagnosed with a partial tear of the calcaneal tendon. The patient received physical therapy alongside other treatments including immobilization, custom orthotics, and platelet rich plasma injections. Despite the conservative treatments performed, symptoms prevailed, and arthroscopic surgery was recommended for calcaneal tendon repair. Before pursuing the recommended surgical treatment, the patient sought a second opinion. At this time, the patient reported pain onset after engaging in physical activity and occasional difficulty moving his big toe. The patient also reported similar pain with palpation and isolated plantarflexion movements. Results of an MRI resulted in a diagnosis of ASM, and surgery was performed to excise the anomaly. During surgery, it was discovered that the patient’s neurovascular bundle was being compressed by the ASM. The surgical excision of the ASM was successful, but recovery was complicated by a flexor hallusis longus rupture. In addition, the authors discussed the two theories for ASM-associated pain including exercise-induced compartment syndrome and muscle claudication.
Collins and Gilden [14] described a triathlete experiencing chronic exertional compartment syndrome (CECS), which is characterized by exercise-induced muscle pain and intra-compartmental pressure build up in the lower legs. Symptom alleviation was achieved through physical therapy over four months, including functional manual therapy, alleviating myofascial restriction, and improving neuromuscular function. The authors identified other cases with similar symptoms to CECS which were treated successfully with physical therapy including functional manual therapy as a non-surgical alternative for ASM treatment.
Plečko et al. [15] described two ASM case reports. The first case report described a 25-year-old female with posteromedial ankle pain, swelling, and no history of trauma reported. The patient initially noticed painless posteromedial ankle swelling which progressed to infrequent pain and swelling during and after running. As time progressed, the patient reported pain in the ankle region when walking and during the night. During the patient's physical exam, pain was provoked in the right ankle when standing on her toes. Throughout the patient’s assessment, ankle range of motion was within the normal range with no indications of ankle instability or impingement. Furthermore, there was indication of an obliterated Kager’s fat pad with no signs of bony deformities or malalignment on a plain radiograph. The diagnosis was confirmed as ASM via MRI and the muscular anomaly was excised. The patient returned to her previous level of activity with no report of pain or complications six months after surgery.
In the second case report, Plečko et al. [15] described a 31-year-old patient with ankle pain, foot pain, and paresthesia. The authors reported no signs of swelling or history of trauma. The patient was reportedly misdiagnosed by various physicians, including a rheumatologist and a musculoskeletal radiology specialist. The patient underwent conservative therapies including NSAIDs, intravenous corticosteroids, and rest without symptom relief. The patient was eventually diagnosed with complex regional pain syndrome and prescribed lidocaine patches and physical therapy. The patient’s pain continued, and she was referred to an orthopedic surgeon, who prescribed opioids, pregabalin, and a referral to hyperbaric chamber therapy. Although the patient felt an improvement in sensation in her right foot, her ankle pain continued. After further assessment by the orthopedic surgeon, the patient’s MRI was revisited and a provisional diagnosis of ASM was made. TTS was confirmed through electromyoneurography (EMNG) and the patient was scheduled for surgery. The ASM was excised, and recovery included non-weight bearing with crutches for two weeks, followed by weight-bearing as tolerated and ankle mobility exercises. The patient gradually returned to her activities of daily living 10 weeks after surgery and was cleared for all activity. The patient reported no symptoms at her 6 month follow-up..
Woo et al. [16] described a young soldier who presented with posteromedial ankle pain and was eventually diagnosed with ASM. The diagnosis was associated with TTS due to exertional compartment syndrome, despite the absence of abnormal electrophysiological findings. The ASM was surgically removed in the right ankle due to the patient’s desire to return quickly back to normal athletic function. After recovery, the patient received reassessments at 12 and 24 months where he reported pain-free return to normal activity levels and resolution of symptoms.
Most ankle problems result from anatomic disorders or abnormal function of articular or extra-articular structures. Less commonly, ankle problems reflect a systemic disorder. ASM anomalies are present in 0.7% - 10% of the population [5,7]. A PubMed search for “accessory soleus” from 2013-2023 resulted in 15 published articles that highlight clinical presentation, current diagnostic practices, and treatment options. Clinical research on the topic is limited in scope and most articles conclude that surgical intervention is the best option for symptomatic ASM [6,7,9,11,13,15].
ASM can be identified via MRI, CT scan, US, surgical intervention, or cadaver studies with no common database for reporting [5,6,11,13,15]. The most common symptoms are pain and discomfort in the posteromedial aspect of the ankle for symptomatic ASM, and a bulging mass and swelling for both symptomatic and asymptomatic ASM [7,9-14,16]. Clinical cases of ASM were documented and the ASM that were surgically removed resulted in resolution of pain and discomfort according to Plečko et al. [15] and Woo et al. [16].
This paper proposes that a delay in diagnosis and subsequent delay in care of patients with posteromedial ankle pain and swelling can lead to unnecessary pain and suffering and increase cost of care. A more timely and accurate diagnosis of posteromedial ankle pain and swelling could be achieved with use of the proposed clinical decision-making flowchart (Figure 2). Using the clinical decision-making flowchart, clinicians can potentially arrive at a more accurate diagnose of posteromedial ankle pain and swelling leading to less pain and suffering, decrease in cost of care, and improved patient outcomes.
ASM diagnoses tend to be made using MRI, and occasionally US, as noted by Luck et al. [11] and Gentile et al. [13] ASM is commonly misdiagnosed due to the limited number of published articles and several authors propose that ASM should be added to the list of differential diagnoses when dealing with swollen ankle(s), pain in the posteromedial aspect of ankle, TTS, and ECS [7,9-12,14,16].
A paucity of studies include the use of conservative methods, such as physical therapy, in the treatment of ASM [10,12,14]. Further, specific rehabilitative interventions have not been fully delineated. As described by Bojinca et al. [10], Doda et al. [12], and Collins and Gilden [14], the cost-effective and non-invasive nature of non-surgical treatment modalities makes them valuable clinical tools to include in ASM treatment. Thus, further investigation into the potential of physical therapy and other non-surgical treatment modalities to alleviate ASM symptoms is warranted. Gentile et al. [13] exemplifies a lack of conservative treatment approaches once the source of the pain was correctly identified, despite prior several non-surgical treatments indicated for prior incorrect diagnoses were considered and carried out.
Conservative measures seem to be especially beneficial for reducing symptoms in patients who are more likely to require a fasciotomy. Further research is needed to expand understanding of physical therapy as an intervention in vulnerable populations since current literature mostly records fasciotomy of ASM in young, athletic patients. Additionally, Doda et al. [12] notes that physical therapy did not return the patient with ASM to their prior level of function. Therefore, further research comparing physical therapy outcomes to surgical intervention in restoring ASM patient prior level of function may prove useful.
Future clinical research on this topic might examine how conservative methods such as manual therapy or biophysical agents might be used to treat ASM as investigated by Collins and Gilden [14], to reduce surgical referral immediately after the ASM diagnosis is confirmed. Also, Rubio et al [17] suggest orthotics to encourage better lower limb alignment and activity modification as needed. Additionally, given that ASM is often misdiagnosed when an MRI test has not been performed, development of educational materials for health care providers regarding the common symptoms of ASM when managing patients with posteromedial ankle pain, TTS, and ECS should be added to the list of differential diagnoses mentioned by Carrington et al. [7], Bojinca et al. [10], Doda et al. [12], Plečko et al. [15], and Woo et al. [16]. In addition, healthcare providers should use an MRI test to rule out ASM rather than potentially misdiagnosing patients and prescribing ineffective treatments, as highlighted by the second case report of Plečko et al.15
Finally, the authors of this study proposed a clinical decision making flowchart for symptomatic ASM for the purpose of facilitating further discussion regarding clinical practice guidelines for possible ASM cases (Figure 2).
The purpose of this article was to review current literature on ASM and to add to the existing body of research on the topic. The authors of this article agree that ASM should be added as a differential diagnosis for posteromedial ankle pain and the other earlier discussed symptoms since ASM signs and symptoms can often resemble other diagnoses, leading to unresolved symptoms. Furthermore, the authors suggest that further research is necessary to explore alternative treatment methods, including physical therapy. Though surgical intervention has been successful in treating the ASM in previous cases, the clinical implications of a non-surgical treatment method may result in less risk to the patient, decrease the financial strain of prolonged disability, and serve as the only possible intervention in cases where surgery is not feasible.