Anatomy and Relevant Structures in Plantar Heel Pain
Introduction[edit | edit source]
Plantar Heel Pain (PHP) is a poorly understood, complex condition. During previous lectures in this series, Plantar Heel Pain Syndrome (PHPS) was introduced, the available literature on the risk factors, assessment and treatment of it explored and a new protocol for the management thereof introduced. In order to optimally manage PHPS, it is imperative to examine the anatomical structures underlying the calf and foot area in order to establish the relationship between PHP and the tissues involved. In this document, the muscular, nervous and facial structures underlying the foot and ankle will be explored in relation to:
- Previous theories on PHPS (including Plantar Fasciitis and Calcaneal Spurs)
- The “new protocol” for the management of PHPS
Anatomical Structures Related to PHPS Theories[edit | edit source]
Plantar Fascia[edit | edit source]
Fascia consists of sheets of connective tissue that form a continuous network through the whole body. It is a collagen-based tissue that attaches, stabilise, impart strength, enclose different organs, support internal structures and envelope whole muscles as well as each individual muscle fibre. Fascia can be classified as superficial, deep, visceral or parietal and is often further classified based on anatomical location. Fascial thickness varies from very thin, almost transparent to strong and thickened.
The fascia of the foot consists of fibrous connective tissue that functions to separate, support and attach muscles. It can also be divided into the superficial and the deep fascia. On the plantar side of the foot, the superficial fascia is involved in the formation of the plantar fat pad whereas the deep layer, known as the plantar fascia, plays an essential role in maintaining the medial longitudinal arch of the foot.
The plantar fascia (PF), also known as the plantar aponeurosis, originates proximally at the medial tubercle of the distal calcaneus and broadens as it extends distally (Figure 1). Distally, at the metatarsophalangeal joints, it divides into five digital slips to each of the toes which fuse with the fibrous flexion sheaths and with the deep transverse metatarsal ligaments in each of the toes before inserting at the base of the proximal phalanges. Besides its support of the longitudinal arch of the foot, the PF is also involved in the mechanisms of propulsion, transmitting the forces and stresses in the foot during loading (shock-absorbing).
It is worth noting again that the plantar fascia is distal to the painful area in the heel commonly reported in PHPS, which raises the question as to whether it can be a causative factor in PHPS.
Plantar Fasciitis[edit | edit source]
Microtrauma caused by excessive tension to the PF is commonly thought to be the source of pain in this syndrome. The Windlass test has been proposed as an assessment technique in the diagnosis of plantar fasciitis with its proposition that passive lengthening of the plantar fascia by extension of the big toe can produce pain in the heel (Figure 2).
This assumption was further studied by Fessel et al  who assessed the function of the PF in various phases of gait and concluded that the “windlass effect” for support of the arch is questionable due to the substantial muscle contribution to support the longitudinal arch (Figure 3).
In an anatomical dissection study of the PF, Stecco et al  identified three parts to the PF - medial, central and lateral - with the central part being the thickest. All dissections revealed that the:
- PF continued over the calcaneal bone with a thin band corresponding to the periosteum of the calcaneal bone
- This layer of the PF surrounded the calcaneus and was continuous with the paratendon of the Achilles Tendon
Further microscopic study revealed the presence of Pacini and Ruffini corpuscles inside the PF, which suggests that plantar fascia innervations have a role in proprioception and in the stability and control of foot movements.
Stecco et al  further raised the question of whether the plantar fascia is indeed a fascia or if it is an aponeurosis. These terms are generally used interchangeably in various studies.
Fascia - tissue with a multidirectional arrangement of the collagen fibres
Aponeurosis - tissue with a unidirectional arrangement of the collagen fibres
In their anatomical study, Stecco et al found that even though the collagen fibres of the PF were mainly arranged in a proximal-to-distal longitudinal direction, various fibres also lay in vertical, transverse and oblique directions. They concluded that this multilayer configuration of the collagen fibres is more typical of fasciae and that the term “plantar fascia” would therefore be a more appropriate term for this tissue.
Besides the structure of the PF, a more pressing question is whether the PF could actually be a source of the pain reported in PHPS. Currently, no evidence could be found of the existence of nociceptive nerve endings in the PF itself but it has been suggested that performing a long stretch, for example with neurodynamic testing, the facial tissue will be stretched in addition to the neural tissue as both of these systems are continuous through the body. There is no doubt that neurodynamic tests not only load the nervous system but also challenge non-neural structures.
Following this concept, Coppieters et al. studied the impact of neurodynamic testing (Slump and Straight leg raise [SLR]) on the perception of experimentally induced pain to assess whether stress on the fascia could be an alternative explanation for changes in pain perception during neurodynamic tests. They injected hypertonic saline into the tibialis anterior muscle of 15 asymptomatic volunteers in order to add strain to the fascia and performed the SLR and slump neurodynamic tests while prohibiting and monitoring all other movements of the ankle (Figure 4).
Coppieters et al. found no change in the perception of experimentally induced pain with the SLR and Slump neurodynamic tests and concluded that these neurodynamic tests have no impact on pain perception when the pain is not of neural origin (Figure 5).
These findings were supported by Coppieters et al. in another study that investigated whether any mechanical movements occurred in the fascia and nerves when performing a modified SLR manoeuvre. They inserted gauges into the sciatic, tibial and plantar nerves as well as the PF of 8 embalmed cadavers to measure the strain during a modified SLR test and found that even though there was significant movement in the tibial nerve in the tarsal tunnel during the modified SLR tibial manoeuvre, no movement occurred in the PF (Figure 6).
The results of this study are surprising considering the long stretch on the fascia. This brings us back to the previously asked question considering the cause of the reproduced heel pain with two standard tests - the heel raise and the mini squat (Figure 7). Both weight-bearing on the heel and stretch on the fascia can hereby be mostly excluded as reasons for the PHP elicited.
Figure 7. Reasoning for reproduced heel pain with standard tests 
In summary of all the evidence gathered for the involvement of the PF in PHPS over the course of the various lectures on heel pain, support could only be found for the thickening of the PF in PHPS (Figure 8).
Figure 8. Summary of the evidence for the involvement of the Plantar Fascia in PHPS (- refers to no support in the literature while + indicates support in the literature) 
Calcaneal Spurs[edit | edit source]
Plantar Calcaneal Spur has been widely implicated as a cause of plantar fasciitis but it remains controversial whether the calcaneal spur actually contributes to the symptoms of PHP. Considering the previous review on the risk factors for PHPS, calcaneal spurs are generally considered as incidental findings as they are not located in the weight-bearing area of the heel and have also been found in asymptomatic individuals. No clear connection, therefore, exists between the presence of calcaneal spurs and PHPS.
Anatomical Structures Related to the “New Protocol”[edit | edit source]
Many structures have been eliminated as possible sources of the heel pain reproduced with the heel raise and mini squat tests, which necessitates considering if the source of pain could be muscular instead (Figure 9)?
Figure 9. Possible sources of the heel pain reproduced with clinical tests 
Muscular System[edit | edit source]
Of the five layers of soft tissue in the foot, four does not cover the heel (Figure 10). Only the superficial layer covers the heel with the fat pad, which has very little nociceptive innervation and has not been proven as a source of pain in the heel. Considering that all the muscles running from the calf to the foot bypass the heel to enter the foot more distally and that there are no muscles in the heel itself, the muscular system can be eliminated as a source of the PHP. With no evidence for the muscles as a source, only the neural tissues are left to be considered (Figure 11).
Figure 10. Five layers of soft tissue in the foot 
Figure 11. Reasoning around the muscles as a source for the PHP with the clinical tests 
Neural Tissues[edit | edit source]
Before exploring the neural tissue of the foot, it is worth revisiting the results of the pressure pain threshold tests performed by Saban & Masharawi  in PHPS. Their results indicate that even though the presentation and sensitivity of the heel pain were not significantly different between individuals with PHPS and those without, the distal medial heel was the most sensitive area in the heel. When considering the neural anatomy of the foot, it is of interest to note that the entrance of the medial and lateral plantar nerves into the foot coincides with this reported area of increased sensitivity in the heel (Figure 12).
Figure 12. Similarities of the PPT test sensitivity and the neural anatomy 
The tibial nerve passes through the fibrous tarsal tunnel before splitting into the medial and lateral plantar nerves. In this part of its course, the tibial nerve is very superficial as it is wedged between the bone and the skin with no other protection. Palpation of the nerve will easily evoke paraesthesia similar to palpation of the ulnar nerve at the elbow. From here, the medial and lateral plantar nerves and the medial calcaneal nerve branch of the tibial nerve together with the arteries and veins enter the foot close to the medial calcaneal tubercle.
Cutaneous innervation of the foot is supplied by 7 different nerves altogether (Figure 13):
- Saphenous nerve (L3,4)
- Deep peroneal nerve (L4,5)
- Superficial peroneal nerve (L4, S1)
- Medial plantar nerve (L4,5)
- Lateral plantar nerve (S1,2)
- Medial calcaneal branch of the tibial nerve (S1,2)
- Sural nerve (S1,2)
In relation to PHPS, the nerve that is of greatest interest is the medial calcaneal nerve. The medial calcaneal nerve is one of the main branches of the tibial nerve and generally separates from the tibial nerve below the medial malleolus around the area of the tarsal tunnel. From here it enters the heel from the medial side before terminating in the skin of the heel, providing sensory innervation to the skin of the heel area (Figure 14).
Figure 14. Medial calcaneal nerve branch of the tibial nerve
Other researchers have also investigated the involvement of the neural tissues in PHPS:
- 2 studies using nerve conduction tests of the plantar nerves 
- a review of heel pain from neural origin 
David Butler  also mentioned the increase in evidence of a peripheral neurogenic contribution to some heel spurs, either from the medial calcaneal nerve or the lateral plantar nerve.
“Heel spurs are also one pain state where the exact pain may not be replicated on physical evaluation, but on neurodynamic testing there are clues that something is not quite right. This could be minimal restrictions in range of motion, or symptoms evoked on the problem side but not the “good” side” - David Butler 
He further suggested treating PHPS with neurodynamic manoeuvres, specifically combining the SLR test with dorsiflexion/eversion of the ankle.
Both nerve conduction studies by Öztuna et al. and Rose et al. assessed the medial plantar nerve (MPN), while Öztuna et al. also investigated the lateral plantar nerve (LPN), and Rose et al. the medial calcaneal nerve (MCN) in order to observe any differences in nerve conduction between these nerves (Figure 15).
Both studies reported disturbances in nerve conduction of these nerves. Öztuna et al. found a difference in nerve conduction between individuals with PHPS and those without and reported that 88% of participants had disturbances in nerve conduction of the MPN and LPN combined. Rose et al. found disturbances in nerve conduction of the MCN in 72% of participants (Figure 16).
Rose et al  further suggest that the reduction in nerve conduction velocity was caused by pressure on the nerve somewhere along its course down the leg before reaching the foot/heel. This supports the findings of Coppieters et al. of the involvement of the neural tissue in PHPS as seen during the modified SLR neurodynamic test with tibial nerve bias. It is also interesting that a nerve block to the posterior tibial nerve is suggested as a treatment option for individuals suffering from severe PHP, which further supports the involvement of the nerves in creating this PHP.
The theory of pressure on the tibial nerve necessitates further study of its course down the leg. After exiting the popliteal fossa, the tibial nerve travels down the posterior leg in-between the superficial and deep muscles of the calf where the muscles could potentially cause pressure on the nerve. These are the same muscles found to be stiff, incompliant and painful on manual palpation in the study by Saban & Deutscher  which suggests that they might in fact be disrupting the conduction of the nerve along its course (Figure 17). On the cross-sectional image of the calf it is clear how intertwined the nerves and muscles are which highlights the possibility of the muscles putting pressure on the nerve (Figure 18).
Figure 17. Course of the Tibial nerve
Figure 18. Cross-sectional image of the lower leg
Conclusion[edit | edit source]
It remains unclear where the first dysfunction would appear in this interaction between the nerves and the muscles. Did the:
pain in the foot ⇒ patient walk differently ⇒ dysfunction of the muscle ⇒ disturbance of the nerve
Or did it happen the other way around? Even though the sequence of events might still be unknown, it is clear that there is a treatment available and the treatment is supported by sound theory. The next lecture in this series will specifically look at the treatment options proposed in the new protocol.
References[edit | edit source]
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