The Effect of HyProCure^® Sinus Tarsi Stent on Tarsal Tunnel Compartment Pressures in Hyperpronating Feet

Article Outline

• Abstract
• Materials and Methods
• Results
• Discussion
• Acknowledgment
• References
• Copyright

Abstract 

Tarsal tunnel syndrome is characterized by increased pressure in the tarsal tunnel. In hyperpronation, there is excessive abnormal pronation resulting from partial displacement of the talus on the calcaneus. In this study, we hypothesized that hyperpronation caused by talotarsal instability will lead to increased pressure in the tarsal tunnel and porta pedis. We also hypothesized that the pressure in these compartments will decrease following an extra-osseous talotarsal stabilization procedure using HyProCure^®. Pressures in the tarsal tunnel and porta pedis were measured in 9 fresh-frozen cadaver specimens using an intracompartmental pressure monitor system. Pressures were measured with the foot in neutral and hyperpronated position, before and after stabilization using HyProCure. For the tarsal tunnel, pressure in the neutral position with and without HyProCure was 3 ± 3 mm Hg and 4 ± 3 mm Hg, respectively (P = .159). However, for the hyperpronating foot, the pressure decreased from 32 ± 16 mm Hg to 21 ± 10 mm Hg (P < .001) following the placement of HyProCure. In the porta pedis, pressure in the neutral position with and without HyProCure was 2 ± 2 mm Hg and 2 ± 2 mm Hg, respectively (P = .168). However, for the hyperpronating foot, the pressure decreased from 29 ± 15 mm Hg to 18 ± 11 mm Hg (P < .001) following the placement of HyProCure. The pain caused by compression of the posterior tibial nerve in the tarsal tunnel and its branches in the porta pedis, owing to hyperpronation, may be alleviated by implantation of HyProCure.

Level of Clinical Evidence: 5

Keywords: arthroereisis, porta pedis, posterior tibial nerve, pressure, pronation, tarsal tunnel syndrome

The term “tarsal tunnel syndrome,” coined by Keck (1) and Lam (2) in 1962, is described as the entrapment of posterior tibial nerve (PTN) and its branches in the tarsal tunnel formed by the flexor retinaculum at the medial ankle and hindfoot 3, 4, 5, 6. The most commonly reported symptoms of this condition are pain, paresthesias, and abnormal sensation in the medial hindfoot and the plantar aspect of the foot 3, 6. A variety of causes of tarsal tunnel syndrome have been described in the literature. In most cases, the etiology is idiopathic. Space-occupying lesions, such as tumors or varicosities, joint hypermobility, pes planus, heel varus and valgus (which may cause tension on the PTN), increased pressure on the PTN (hyperpronation may cause tension on the flexor retinaculum, thus altering the volume of the tarsal tunnel and hence the pressure), rapid weight gain, ankle sprains, and fractures of the ankle joint may lead to tarsal tunnel syndrome 5, 6, 7, 8, 9, 10. Based on the underlying cause, the symptoms associated with tarsal tunnel syndrome may be relieved by physiotherapy, activity modification, and the use of orthotic insoles 5, 6, 8. Following the failure of conservative measures, operative release of the flexor retinaculum is considered when pressure in the tarsal tunnel is increased owing to space-occupying lesions and reduced cross-sectional area caused by talotarsal instability 3, 5, 8, 11.

Hyperpronation or excessive pronatory motion of the foot occurs because of talotarsal instability 12, 13. This leads to subluxation (adduction and plantarflexion) of the talus on the calcaneus and excessive pronation of the foot 12, 13, 14, 15. Abnormal foot biomechanics and joint hypermobility produce traction injury to the PTN or direct compression trauma by the flexor retinaculum and its surrounding structures 1, 6, 16, 17. It has been shown that increased pressure on nerves reduces intraneural blood flow and causes nerve damage. Increased pressure is known to have detrimental effects on nerve conduction, axonal flow, neural ischemia, and local nerve demyelination 18, 19. Previous studies have shown a significant decrease in the tarsal tunnel compartmental volume with the foot in maximum eversion or inversion, as compared to the foot in a neutral position (10). In recent studies by Trepman et al (7) and Barker et al (20), it was shown that pressures in the tarsal tunnel, and the medial and lateral plantar tunnels, increases significantly with changes in foot and ankle position. The intracompartmental pressure in the tarsal tunnel was found to increase significantly with the foot held in dorsiflexion, plantarflexion, supination, and pronation 20, 21, 22.

The HyProCure sinus tarsi stent (GraMedica, Macomb, MI) is an extra-osseous talotarsal stabilization device that prevents abnormal closure of the sinus tarsi, therefore restoring the normal triplanar motion while eliminating excessive motion of the talus on the calcaneus 13, 23. HyProCure, composed of medical-grade titanium alloy, is placed via a minimally invasive operative procedure. The positioning of this device follows the alignment of the sinus tarsi, ie, from anterior-distal-lateral to proximal-medial-posterior (Figure 1) when compared with other internal devices that are inserted purely lateral to medial 24, 25. HyProCure is placed within both the sinus and canalis portions of the sinus tarsi, whereas other devices are placed only in the outer 50% of the sinus tarsi. Owing to the inherent shape of HyProCure, the middle tapered portion of the device abuts the lateral part of the canalis tarsi to ensure proper placement and to prevent overinsertion. An appropriate-size HyProCure restores the normal range of pronatory motion. It is acknowledged that an internal bone stabilization device that eliminates excessive pronatory motion and helps support the medial longitudinal arch of the foot can have a positive outcome in patients suffering from tarsal tunnel syndrome 7, 8.

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• Fig. 1 

  Placement of HyProCure sinus tarsi stent in alignment with the sinus tarsi and abutting the lateral part of the canalis tarsi. Reproduced with the permission of GraMedica, LLC.

The goal of our study was to quantify the pressure in the mid section of the tarsal tunnel and the porta pedis with the foot held in the neutral and maximally pronated position, before and after talotarsal stabilization using HyProCure. The posterior tibial nerve bifurcates in the tarsal tunnel at the level of the ankle and then enters into the plantar aspect of the foot at the abductor canal. This canal is traditionally referred to as the porta pedis and lies below the superior boundary of the fibrous edged openings in the abductor hallucis muscle 6, 8, 26. The porta pedis is known as an area of extreme constriction and plays a significant role in producing symptoms associated with tarsal tunnel syndrome (6). There have been no reports of pressure measurements in the porta pedis in cadavers, or in patients diagnosed with tarsal tunnel syndrome. Also, we found no reports of pressure measurements in the tarsal tunnel or porta pedis following the stabilization of the talotarsal joint complex. We hypothesized that pressures in the tarsal tunnel and porta pedis would increase significantly with the foot held in maximum pronation (ie, hyperpronation) as compared with the foot held in a neutral position with mild plantarflexion (for both with and without HyProCure). We also hypothesized that following talotarsal stabilization using HyProCure the pressures in the tarsal tunnel and porta pedis would decrease significantly in the maximally pronated position (in comparison with pressures in the maximally pronated position without intervention using HyProCure).

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Materials and Methods 

Nine fresh-frozen human adult cadaver specimens (all female) were used for tarsal tunnel pressure measurements. Each specimen consisted of the foot, ankle, and distal segment of the leg (approximately 20 cm proximal to the ankle joint). Five left-footed and 4 right-footed specimens were used to quantify pressure. All specimens were inspected for their range of motion at the ankle joint complex. Each specimen exhibited hyperpronation. Specimens with previous operative intervention, fracture, or pathologic conditions in the ankle-hindfoot complex were excluded from this study. The specimens were adequately thawed to room temperature before testing. Each specimen was dissected free of soft tissue at the proximal tibial and fibular segment. The proximal segment of leg was potted using polymethylmethacryalte (PMMA) for mounting in the testing fixture (Figure 2). Care was taken to avoid damage to the soft tissue structures of the foot and ankle joint complex.

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• Fig. 2 

  Foot specimen mounted on the materials testing system (MTS). A right-footed specimen mounted on the MTS (used solely for support purposes). The proximal segment of tibia-fibula was potted using polymethylmethacryalte (PMMA) for fixating the specimen to the MTS.

The flexor retinaculum was exposed by longitudinal incisions made in the area of the tarsal tunnel. A similar incision was made on the medial aspect of the plantar surface to expose the porta pedis. The potted specimen was mounted on a material testing system (MTS Bionix 858, Eden Prairie, MN) solely for support purposes (Figure 2). The Stryker Instruments’ 295 Intra-Compartmental Pressure Monitor System (Kalamazoo, MI) was used for making pressure measurements. The pressure monitor system with a breakaway needle and the indwelling slit catheter was held at the level of the flexor retinaculum outside the foot and set to 0 mm Hg. The breakaway needle along with the catheter was introduced into the anterior edge of the flexor retinaculum. The needle was withdrawn and care was taken to avoid abutment of the tip or kinking of the catheter (20). Approximately 0.2 mL of normal saline was injected into the tunnel and the pressure was recorded with the foot held in mild plantarflexion and the ankle in a neutral position (Figure 3). Next, the investigator pronated the foot maximally (hyperpronated) by applying a vertical force under the fourth and the fifth metatarsal head. The foot was held in this position and another 0.2 mL of normal saline was injected into the tunnel following which the pressure was recorded after allowing the reading to equilibrate for approximately 15 seconds (Figure 4). The foot was then unloaded back to neutral; this procedure was repeated 3 times to give 3 readings each for the neutral and hyperpronated positions (ie, n = 3 for each position per foot without HyProCure).

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• Fig. 3 

  Pressure measurement in tarsal tunnel: neutral position. A right-footed specimen in neutral position with the catheter placed in the tarsal tunnel. Following the placement of the catheter the needle was withdrawn and supported on a stand (not shown here). Care was taken to avoid abutment of the tip or kinking of the catheter. Normal saline was injected into the catheter and the reading on the pressure monitor system was recorded after allowing stabilization for approximately 15 seconds.

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• Fig. 4 

  Pressure measurement in tarsal tunnel: hyperpronated position. A left-footed specimen being pronated maximally by application of a vertical force under the fourth and fifth metatarsal head. Notice that the catheter is placed in the tarsal tunnel and the needle is withdrawn. Following maximum pronation of the foot, normal saline was injected into the catheter and the pressure was recorded after allowing it to stabilize.

Following this procedure, a lateral incision was made over the sinus tarsi for insertion of the HyProCure sinus tarsi stent (Figure 5). HyProCure is available in sizes ranging from 5 mm to 10 mm, with increments of 1 mm. These sizes correspond to the outer diameter of the threaded cylindrical portion of the implant. The appropriate HyProCure stent size required to eliminate hyperpronation while maintaining the normal range of pronatory motion was determined using the HyProCure trial sizers. The size of the stent used was dependent on individual foot specimens. For our experiments, we used size 7 in 5 specimens and size 8 in the remaining 4 specimens. Following the implantation of HyProCure, pressure measurements were made in the tarsal tunnel with the foot in the neutral and maximally pronated positions, as described above (again, n = 3 for each position per foot with HyProCure).

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• Fig. 5 

  Insertion of HyProCure. A lateral incision was made over the sinus tarsi in a left-footed specimen. Following the incision an appropriate-size HyProCure (not shown here) was inserted and pressure measurements were made with the foot in neutral and maximally pronated positions.

The HyProCure was then removed and the entire procedure was repeated for measuring the pressure in the porta pedis, ie, pressure was measured in the neutral and maximally pronated position (Figure 6), with and without intervention using HyProCure. The pressure within the porta pedis is not affected by the removal and reinsertion of HyProCure. Removing the device only brings back the pathological talotarsal motion (instability of the talotarsal joint complex), and reinsertion eliminates the pathological instability and restores the normal range of pronatory motion.

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• Fig. 6 

  Pressure measurement in porta pedis. A right-footed specimen in neutral position with the catheter placed in the porta pedis. Pressure measurements were made in the porta pedis with the foot held in neutral and maximally pronated positions, before and after insertion of HyProCure.

A load cell (Honeywell, Columbus, OH) placed under the fourth and fifth metatarsal head was used to quantify the force applied by the investigator while maximally pronating the foot. Forces were quantified both before and after insertion of HyProCure to check for consistency. Throughout the experiment, the investigator was blinded to the output of the pressure monitoring system and the load cell.

The data reported are mean, standard deviation (± 1 SD), and range of pressure values for each experimental condition. The first hypothesis tested was that the pressure in the neutral position (in both the tarsal tunnel and porta pedis) with and without HyProCure will NOT be statistically different (H_a: μ_{HyProCure_Neutral} ≠ μ_{No Treatment_Neutral}). A 2-sided Wilcoxon signed rank test was computed to test for significance at the 95% confidence level.

The second hypothesis tested was that the pressure in the tarsal tunnel and porta pedis will be higher for the foot in a maximally pronated position when compared with the foot in the neutral position (H_a: μ_{Hyperpronated} > μ_Neutral; for both with and without HyProCure). A 1-sided Wilcoxon signed rank test was computed to test for significance at the 95% confidence level.

The third hypothesis tested was that for a hyperpronated foot, the pressure in the tarsal tunnel and porta will decrease following an extra-osseous talotarsal stabilization procedure using HyProCure (H_a: μ_{HyProCure_Pronation} < μ_{No Treatment_Pronation}). Again, a 1-sided Wilcoxon signed rank test was computed to test for significance at the 95% confidence level. For all 3 tests, the null hypothesis of no difference was rejected for P values less than .05. All statistical analyses were performed using SigmaStat v3.5 (Point Richmond, CA) and Microsoft Excel.

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Results 

The load applied by the investigator under the fourth and fifth metatarsal head (for maximally pronating the foot) was consistent. The measured force was found to be 116 ± 10 N and 115 ± 14 N (mean ± 1 SD, n = 27) for with and without HyProCure, respectively. The applied force was not statistically different. A 2-tailed paired t test resulted in a P value of .797.

The pressures measured in the tarsal tunnel with the foot in neutral and hyperpronated positions, with and without implantation of HyProCure, are shown in Table 1. As expected, the pressures in the neutral position with and without HyProCure were not statistically different. A 2-sided Wilcoxon signed rank test resulted in a P value of .159. The pressures in the tarsal tunnel with the foot held in a maximally pronated position were significantly higher as compared with the foot in a neutral position, for both with and without HyProCure, having P values less than .001 (1-sided Wilcoxon signed rank test). With the insertion of HyProCure, the pressure in the tarsal tunnel decreased from 32 ± 16 mm Hg to 21 ± 10 mm Hg (mean ± 1 SD) for a maximally pronated foot, ie, the pressure decreased by 34% (Figure 7). This decrease in pressure was found to be statistically significant with a P value less than .001 (1-tailed Wilcoxon signed rank test).

Table 1. Tarsal tunnel pressures (N = 27)

Table 1 shows average (n = 3) pressure measurements in (mm Hg) in the tarsal tunnel with the foot held in neutral and maximally pronated positions for each of the 9 foot specimens, with and without intervention using HyProCure. Each data value is an average of 3 readings to give a total sample size of n = 27. The column on the extreme right represents the percentage reduction in pressure following the insertion of HyProCure with the foot held in maximally pronated position. The range and 95% confidence interval (CI) of reported values were obtained from the raw data.

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• Fig. 7 

  Graphical representation of pressure readings in a hyperpronated foot in the tarsal tunnel and porta pedis, with and without intervention using HyProCure. The error bars represent ± 1 Standard Error of Mean (SEM). ^∗Indicates a statistically significant decrease in pressure with P < .001.

Similarly, the pressures measured in the porta pedis with the foot in neutral and hyperpronated positions, with and without implantation of HyProCure, are shown in Table 2. Again, the pressures in the neutral position with and without HyProCure were not statistically different. A 2-sided Wilcoxon signed rank test resulted in a P value of .168. The pressures in the porta pedis with the foot held in a maximally pronated position were significantly higher as compared with the foot in a neutral position, for both with and without HyProCure, having P values less than .001 (1-tailed Wilcoxon signed rank test). With the insertion of HyProCure, the pressure in the porta pedis decreased from 29 ± 15 mm Hg to 18 ± 11 mm Hg (mean ± 1 SD) for a maximally pronated foot, ie, the pressure decreased by 38% (Figure 7). This decrease in pressure was found to be statistically significant with a P value less than .001 (1-tailed Wilcoxon signed rank test).

Table 2. Porta pedis pressures (N = 27)

Table 2 shows average (n = 3) pressure measurements in (mm Hg) in the porta pedis with the foot held in neutral and maximally pronated positions for each of the 9 foot specimens, with and without intervention using HyProCure. Each data value is an average of 3 readings to give a total sample size of n = 27. The column on the extreme right represents the percentage reduction in pressure following the insertion of HyProCure with the foot held in maximally pronated position. The range and 95% confidence interval (CI) of reported values were obtained from the raw data.

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Discussion 

Tarsal tunnel syndrome has traditionally been a somewhat mysterious disease process. There are a multitude of etiological factors named as the cause of paresthesias, abnormal sensations, and pain along the distribution of posterior tibial nerve fibers extending from a region posterior to the medial malleolus down to the toes. Because of the lack of a true diagnosis, this syndrome is usually considered to be idiopathic. On further investigation/questioning of the patient suffering from the ill effects of this condition, it is usually discovered that the symptoms worsen after periods of weight bearing, indicating an underlying biomechanical etiology. Many times conservative treatments are unable to alleviate the symptoms, leading to the consideration of surgical options. Also, surgical decompression of the tarsal tunnel alone has not been proven to be extremely effective. The true etiology of the disease process, i.e., abnormal foot biomechanics, must be addressed to reduce the symptoms. The use of an internal stabilization device to restore the normal biomechanics of the hindfoot structures is paramount.

The authors have shown that an extra-osseous talotarsal stabilization using HyProCure was effective in significantly reducing pressures in the tarsal tunnel and the porta pedis for a hyperpronated foot. This is the first study to report direct intracompartmental pressure measurements in the tarsal tunnel and porta pedis following the stabilization of talotarsal joint complex. It follows from this that for a hyperpronating foot, tarsal tunnel syndrome may be relieved by stabilization of the talotarsal complex using the HyProCure sinus tarsi stent. Stabilization will lead to elimination of the excessive pronatory motion of the foot and hence reduced pressures in the tarsal tunnel and porta pedis.

The range of pressure measurements obtained in this study are in good agreement with the values reported in the literature. In human cadaver specimens, Trepman et al. (7) recorded a mean (range) pressure of 2 (0 to 7) mm Hg with the foot in a neutral position as compared with 32 (12 to 60) mm Hg in the everted and 17 (0 to 40) mm Hg in the inverted positions. Kumar et al (22) recorded pressures in the tarsal tunnel of human subjects in the range of 4 to 6 mm Hg with the foot in neutral position, which increased to 10 to 15 mm Hg during plantarflexion and 10 to 20 mm Hg during dorsiflexion of the ankle joint. Barker et al (20) and Rosson et al (21) conducted a series of experiments in which they measured pressures in the tarsal, medial plantar, and lateral plantar tunnels. In a study done in 2007 in human adult cadaver specimens, Barker et al (20) reported a mean tarsal tunnel pressure of 3.5 (1 to 6) mm Hg with the foot in a neutral position. Pressure in the tarsal tunnel was found to be significantly elevated with the foot in maximal pronation, which decreased significantly following an operative decompression procedure: 9.36 (1 to 33) mm Hg and 2 (1 to 4) mm Hg, respectively (20). In Rosson et al’s recent study published in 2009 (21), they measured pressures intraoperatively in 10 patients diagnosed with tarsal tunnel syndrome. With the foot held in pronation, they reported a predecompression mean pressure value of 4.5 (0 to 47) mm Hg in the tarsal tunnel; after decompression, this pressure decreased to 1.5 (0 to 4) mm Hg. Also, the pressures measured in live human subjects were similar to those in the cadaver specimens (21).

A critical factor in the treatment of tarsal tunnel syndrome is to reduce the pronatory forces acting on the flexor retinaculum and abductor hallucis brevis. In the present study we report a significant decrease (P < .001) in pressure in the tarsal tunnel and porta pedis following the implantation of HyProCure in hyperpronated feet (Table 1, Table 2, Figure 1). Our hypothesis that pressures in these 2 areas will be higher in maximum pronation as compared with the neutral position was found to be true and in agreement with the literature 7, 20, 21. Our second hypothesis that pressures would decrease following the stabilization of talotarsal joint complex with HyProCure device is supported by the measured data. We speculate that this decrease is the result of the elimination of excessive abnormal pronation because of insertion of the HyProCure, which then reduces the compressive force applied by the flexor retinaculum on the posterior tibial nerve compartment. It is noteworthy to mention that the porta pedis is an area of extreme constriction. Many surgeons treat tarsal tunnel syndrome by performing decompression procedure on the flexor retinaculum without considering the fact that the bifurcated nerve may be crushed within the porta pedis. This leads to a failed decompression operative treatment and the symptoms of tarsal tunnel syndrome continue to occur, causing pain and discomfort to the patient (6). However, with the insertion of HyProCure, pressure decreases significantly in the porta pedis as well. We speculate that this decrease in pressure is a result of reduction in the compressive force applied by the abductor hallucis brevis muscle (which forms the roof of the porta pedis) to the nerves passing through the porta pedis and into the plantar aspect of the foot. As mentioned previously, increased pressure on the nerve interferes with intraneural blood flow (18) and a pressure of 20 to 30 mm Hg has been shown to impair venular flow in the tibial nerve in rabbits (19). Following talotarsal stabilization using HyProCure, the pressure in the tarsal tunnel and porta pedis decreased below this range in maximally pronated feet.

Previous studies have mentioned that abnormal foot biomechanics may contribute to tarsal tunnel syndrome, and that correction using orthotic support devices may be helpful in reducing the symptoms 16, 27, 28; however, we did not find any study that showed direct evidence of reduction in tarsal tunnel pressure following treatment using an orthotic support device. Also, Edwards et al (29) and Mann (30) mention that conservative treatment (such as orthotics) used to cure tarsal tunnel syndrome are best at temporizing. Again, we would like to stress the point that excessive pronation is initiated by partial displacement of the talus on the calcaneus and the navicular. HyProCure is designed to internally stabilize the talus on the calcaneus; orthotics could actually increase the pressure on the porta pedis to worsen the symptoms. Furthermore, there are other limiting factors of orthotics such as patient compliance issues, limited ability to stabilize the talus on the calcaneus, expense, and so forth.

Many authors believe that valgus heel and abducted forefoot in a flexible flat foot deformity can cause tarsal tunnel syndrome by placing tension on the posterior tibial nerve and its branches 8, 31, 32, 33. Daniels et al (9) found that posterior tibial nerve tension increases during internal rotation of tibia (which occurs during hyperpronation). Francis et al (8) report that a hypermobile flat foot places the posterior tibial nerve and its medial and lateral branches “on the stretch” with each weight-bearing step. They mention that this could be a factor initiating the occurrence of tarsal tunnel syndrome. We speculate that hyperpronation of the foot places strain on the posterior tibial nerve and its branches, and stabilization of the talotarsal joint complex using HyProCure will reduce this strain and hence the symptoms associated with tarsal tunnel syndrome. Research is being conducted to quantify the strain in the posterior tibial nerve in hyperpronating feet to access the effectiveness of HyProCure in reducing this strain.

For the treatment of tarsal tunnel syndrome in mild to moderate cases, it is possible to first try stabilization of the talotarsal joint complex with HyProCure before tarsal tunnel decompression. However, in one of our cadaver specimens we measured a mean pressure of 68 mm Hg in the tarsal tunnel and 64 mm Hg in the porta pedis with the foot held in maximum pronation, without implanting HyProCure. After implantation the pressure reduced to 43 mm Hg and 44 mm Hg in the tarsal tunnel and porta pedis, respectively. The pressure reduced significantly; however, it was still high enough to cause chronic nerve damage (19). This example shows that treatment using HyProCure alone may not be effective in relieving the symptoms caused by tarsal tunnel syndrome, and operative release of the flexor retinaculum may be essential to lower the pressure to an acceptable value. However, transection of the flexor retinaculum alone, to relieve the pressure in the tarsal tunnel, may not necessarily reduce the tension on the nerve caused by hyperpronation, and tarsal tunnel syndrome may still occur (7).

Internal stabilization of the talotarsal joint complex is essential in minimizing the subluxation of the talus on the calcaneus, thus eliminating hyperpronation and reducing the pressures in the tarsal tunnel and the porta pedis. The HyProCure sinus tarsi stent was effective in significantly reducing the pressures in these tunnels by preventing excessive pronatory motion of the foot and ankle joint complex. Walking is the second most common conscious function of the body, and with each step as the foot pronates, pressure is placed on the posterior tibial nerve. With hyperpronation, excessive pressure is placed on the nerve with each step, which accumulates over time and can lead to chronic nerve damage. Lowering the pressures in these tunnels may prevent chronic nerve damage and thus avoid the need for tarsal tunnel decompression. Clinical implications of HyProCure suggest restoration of the normal pronatory motion and hence reduced pressure on the posterior tibial nerve and its branches.

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Acknowledgment 

We thank Manoj K. Kodigudla and Vikas Kaul at the University of Toledo and Avanthi Chikka at Graham International Implant Institute for their help in arranging the experimental set-up and potting of the foot specimens. We also thank Stryker Instruments for providing assistance in the use of their pressure monitor system.

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