The quadratus plantae (QP) is an intrinsic flat quadrilateral muscle located in the second layer of plantar muscles of the foot, and the tendon of flexor digitorum longus (FDL) shares the same anatomical plane as the muscles of the sole’s second layer [1]. Other names used interchangeably for QP include “moles carnea,” “pronator pedis,” “caro plantae pedis quadrata,” “flexor digitorum accessories,” “Massae carnae,” and “caro quadrata” [2]. Nowadays, QP and flexor digitorum accessories are both names that gained popularity among anatomists following the Birmingham Revision in 1933 [2].

There is no hand muscle analogous to the QP. The QP originates from two heads: a smaller lateral head that is evolutionary conserved and a larger medial head. While the lateral head is found in other mammals, the medial head is distinctive to humans [3]. The medial head of QP showed more variability than the lateral head [4]. Athavale et al. [4] found various pattern of the medial head of the QP, from the complete absence to the bulky fleshy origin. Coomar et al. [5] observed that the medial head of QP was inserted into the flexor hallucis longus (FHL) tendon instead of the FDL tendon. Talhar et al. [6] observed, besides QP’s usual two heads, that some muscle fibers of QP were originating from the fascia covering the FHL, and QP was not attached to FDL.

Raviteja et al. [7] observed that in the left foot, QP gave off inter-tendinous connections to the 4th tendon of FDL and also to the second tendon of the flexor digitorum brevis.

The condition of having supernumerary fingers or toes or any complex duplication of any parts is known as polydactyly [8]. It is among the most prevalent birth defects affecting the limb observed immediately at birth.

Anatomical awareness of the musculoskeletal variations associated with polydactyly is essential for anatomists, orthopaedicians, physiotherapists, and surgeons. This study was approved by the Institutional Ethics Committee, AIIMS Jodhpur (Institutional Ethics Committee approval no. AIIMS/IEC/2024/519).

During routine lower limb cadaveric dissection in the Department of Anatomy at All India Institute of Medical Sciences Jodhpur, we found an intriguing case of unilateral polydactyly in the left foot of a 61-year-old male cadaver. During the dissection of the sole as per the instructions in the manual dissection, we observed a relationship between the medial head of QP and the 4th tendon of FDL (Fig. 1). For an accurate assessment of this relationship, QP and the tendons of FDL were carefully dissected up to its insertion to the plantar surface of the base of the distal phalanges. We observed that the medial head of QP gave off an extra tendinous slip before joining the lateral head of QP (Fig. 1). Then, this extra tendinous slip gave a thin tendinous connection to the 4th tendon of the FDL (red arrow; Fig. 1B). The tendon of FDL passed forward as four separate tendons. The medial three tendons of FDL were inserted typically into the plantar surface of bases of distal phalanges of the 2nd, 3rd, and 4th toes, respectively (Fig. 1A). The 4th tendon of the FDL was divided into two tendinous parts after receiving a thin fibrous slip from the tendinous slip of the medial head of QP (Figs. 1, 2). The medial division of the 4th tendon of FDL passed forward and attached to the base of the distal phalanx of the 5th toe (Figs. 1A, 2). The extra tendinous slip from the medial head of QP attached distally to the lateral side of the lateral division of the 4th tendon of FDL and formed a common anomalous tendon to the 6th toe (yellow arrow; Fig. 1B). The anomalous tendon was finally inserted into the plantar surface of the base of the distal phalanx of the extra 6th toe (Figs. 1A, 2).

Additionally, the abductor digiti minimi and flexor digiti minimi brevis muscles were found to be attached to the lateral side of the base of the proximal phalanx of the 6th toe. After removing both the plantar and extensor muscles of the foot, we observed that the 6th toe’s proximal phalanx was articulated with the extra 6th metatarsal head and the base of the 6th metatarsal articulated proximally with the cuboid (Fig. 3). The 5th metatarsal’s base was found sandwiched between the base of the 4th and 6th metatarsals and was not articulated with the cuboid (Fig. 3).

In this case report, polydactyly (extra 6th toe) was observed in the left foot, and the flexor tendon to the 6th toe was derived from both FDL and QP.

Barlow documented a bilateral anomalous variation involving the FDL and QP in a 71-year-old male. In the left foot, FDL was observed to be divided into three tendons instead of four. The medial two tendons were normally attached to the 2nd and 3rd toes, while a small tendon connected to the 4th toe. The lateral two tendons to the 4th and 5th toes originated from the anomalous QP. Meanwhile, a in the right foot, the tendon to the 4th toe received equal contributions from the FDL and QP [9]. In a 75-year-old male, Claassen and Wree [10] also observed an anomalous tendon leading to the 5th toe in both feet, which was related to the QP. In the left foot, anomalous tendon was associated with the medial and lateral processes of the calcaneal tuberosity, whereas in the right foot, with the medial part of the QP [10].

In another study in a male cadaver’s left foot, the second toe’s flexor tendon was derived from QP and the flexor digitorum brevis. QP also gave origin to the medial head of the second lumbrical [6].

According to Nayak and Vasudeva [11], an accessory slip of QP originated from the fascia covering the abductor digiti minimi muscle and was inserted into the FDL. The lateral plantar nerve and vessels are surrounded by this accessory slip of the QP. The lateral plantar nerve may be compressed in this type of variation and might be misdiagnosed as tarsal tunnel syndrome [11].

The QP muscle shows considerable variation regarding its site and pattern of attachment. Pretterklieber [2] observed a one-headed QP in 34%, two-headed in 57%, and three-headed variants of QP in 9%. It has been reported that QP lacks either a medial or lateral head in approximately 20% of the human population, though the complete absence of QP in approximately 2% of the population [12].

Pretterklieber [2] observed three types of QP insertion patterns: muscular, tendinous, and aponeurotic. In the present case, the QP has both muscular and tendinous insertion patterns.

Yamamoto et al. [13] demonstrated that the flexor tendons in human embryos’ foot planta arise from a common tendinous plate just like the hand. This common tendinous plate is developed by joining the FHL and FDL tendons.

Uchiyama et al. [14] observed that, initially, QP was developed at the same level or depth as the FDL. But, QP might occur later in the common tendinous plate itself [14].

Even after birth, some connections between tendons in the tendinous plate seem to persist, potentially leading to a higher prevalence of flexor tendon anomalies in the human foot in comparison to the hand [13].

The derivation of the QP is unclear, but it was assumed that during embryonic development, the entire QP was developed as a part of a single flexor mass of the leg. But, later on, it descends down into the sole and is arranged on the lateral aspect [2].

In our study, we observed an extra 6th digit in the left foot. The extra digit usually lacks muscular connections [15], but in our case, the muscles were attached to the extra 6th toe.

Polydactyly is an extremely heterogeneous condition phenotypically. Polydactyly is more common in the left foot [8]. Postaxial polydactyly is the most common polydactyly type, in which an extra finger is at the lateral side of the 5th finger or toe [8].

Mangalgiri and Sherke [15] reported a case of bilaterally symmetrical polydactyly, where the tendon of flexor digitorum brevis and FDL bifurcated for the 5th and 6th toes and 6th toe articulating with the 5th metatarsal.

Polydactyly typically arises from some underlying genetic disorders, often following autosomal dominant, although the recessive type exists less frequently. It may be manifest as syndromic or non-syndromic variations. The pathophysiology of polydactyly is extremely complex and extends beyond Mendelian inheritance, involving mechanisms such as mutations in various genes, genetic and allelic heterogeneity, the influence of suppressors/enhancers, as well as environmental and developmental factors, including epigenetics [8].

In conclusion, the knowledge of this variation would be beneficial for imaging studies, biomechanical research, and a variety of foot reconstructive surgeries, including correction of congenital deformities like clubfoot and claw toes. Moreover, this awareness extends to the management of conditions like diabetic foot neuropathy and other painful or disabling foot disorders.