Targeted Muscle Reinnervation for a Symptomatic Neuroma in a Traumatic Transmetatarsal Amputee: A Case Report.

CASE: An overall healthy 48-year-old man suffered a left foot mangled crush injury resulting in a post-transmetatarsal amputation and subsequently developing a painful neuroma on the plantar surface of the foot. To avoid the zone of injury, targeted muscle reinnervation was used to treat the neuroma by coapting the tibial nerve to the motor point of the flexor hallucis longus (FHL) muscle. At 1-year follow-up, the patient reported no pain at rest, returned to work, and could ambulate with an orthosis for 30 minutes. CONCLUSION: Rare tibial nerve coaptations to the FHL could serve as a treatment option for patients with neuromas in traumatic postmetatarsal amputation.

Management of an Early-Onset, Painful Tibial Nerve Neuroma Using an Autologous Nerve Graft.

This case report describes the treatment of a postoperative painful neuroma of the tibial nerve using an autologous nerve graft in a dog. The patient presented with sudden non-weight-bearing lameness 10 days after iatrogenic tibial nerve injury during preparation of a reverse saphenous conduit flap. The dog showed severe pain at the surgical site without nerve deficits. A magnetic resonance imaging examination revealed an enlarged tibial nerve at the injury site, consistent with a neuroma. Analgesics were administered over 11 days, but the patient remained in severe pain and non-weight-bearing. Therefore, surgical resection was recommended. The fusiform neuroma was resected microsurgically, and a saphenous nerve graft was transplanted using an epineural nerve repair technique. Histopathological examination was consistent with a neuroma. The dog showed immediate pain relief and weight-bearing the day after surgery with normal motor function. The dog made a full recovery by the last follow-up 6 mo after surgery. If patients develop pain and lameness following surgery or nerve injury, neuroma formation must be considered, even shortly after surgery. Microsurgical resection and autologous nerve transplantation using an epineural nerve repair technique is a viable method to treat painful neuromas and minimize the risk for recurrence in dogs.

Reduced Gene Expression of KCC2 Accelerates Axonal Regeneration and Reduces Motor Dysfunctions after Tibial Nerve Severance and Suturing.

Gamma-aminobutyric acid and glycine (GABA/Gly) are predominantly inhibitory neurotransmitters in the mature central nervous system; however, they mediate membrane potential depolarization during development. These differences in actions depend on intracellular Cl- concentrations ([Cl-]i), which are primarily regulated by potassium chloride cotransporter 2 (KCC2). After nerve injury, KCC2 expression markedly decreases and GABA/Gly mediate depolarization. Following nerve regeneration, KCC2 expression recovers and GABA/Gly become inhibitory, suggesting that KCC2 reduction and GABA/Gly excitation may be crucial for axonal regeneration. To directly clarify their involvement in regeneration, we analyzed recovery processes after tibial nerve severance and suturing between heterozygous KCC2 knockout mice (HT), whose KCC2 levels are halved, and their wild-type littermates (WT). Compared with WT mice, the sciatic functional index-indicating lower limb motor function-was significantly higher until 28 days after operation (D28) in HT mice. Furthermore, at D7, many neurofilament-positive fibers were elongated into the distal part of the sutured nerve in HT mice only, and myelinated axonal density was significantly higher at D21 and D28 in HT animals. Electron microscopy and galanin immunohistochemistry indicated a shorter nerve degeneration period in HT mice. Moreover, a less severe decrease in choline acetyltransferase was observed in HT mice. These results suggest that nerve degeneration and regeneration proceed more rapidly in HT mice, resulting in milder motor dysfunction. Via similar microglial activation, nerve surgery may reduce KCC2 levels more rapidly in HT mice, followed by earlier increased [Cl-]i and longer-lasting GABA/Gly excitation. Taken together, reduced KCC2 may accelerate nerve regeneration via GABA/Gly excitation.

Reversal of cold intolerance by testosterone in orchiectomized mice after tibial nerve transection.

Cold intolerance is a debilitating effect of nerve injury, has a strong impact on the life of patients and no advisable treatment exists against it. Testosterone influences pain pathways and has analgesic effects. A recent study showed testosterone as being an agonist of TRPM8, the predominant ion channel that contributes to cold hypersensitivity after injury. We investigated the effect of testosterone on cold sensitivity after nerve injury. Specifically, using the double plate test (DPT) (thermo-neutral-plate: 31 ºC and cold-plate: 18 ºC) we determined the thermal preference of mice at different points during the study design consisting of: orchiectomy, tibial nerve transection (TNT) (30 days after orchiectomy), 15-days-repeated subcutaneous injections of testosterone enanthate (250 or 500 µg/kg/day) or vehicle (started 12 h after TNT surgery). Different parameters such as time spent on cold plates, distance traveled, animal speed on the cold- and thermo-neutral-plates were determined in naïve, sham and neuropathic animals. Neither orchiectomy nor sham TNT surgery generate effects on cold intolerance and animal activity while TNT surgery decreased the time spent on the cold-plate and the distance traveled during DPT. Testosterone administration reversed the effect of nerve injury, decreasing the cold hypersensitivity and increasing activity of TNT mice. However, the effect of testosterone on cold avoidance reduced with time and at 14 days after TNT surgery, a higher dose was needed to reverse the effect generated by nerve injury. This indicates that although testosterone administration has a positive effect on cold intolerance, it might not be suitable for prolongated treatment.

Short-Duration, Pulsatile, Electrical Stimulation Therapy Accelerates Axon Regeneration and Recovery following Tibial Nerve Injury and Repair in Rats.

BACKGROUND: Repair of nerve injuries can fail to achieve adequate functional recovery. Electrical stimulation applied at the time of nerve repair can accelerate axon regeneration, which may improve the likelihood of recovery. However, widespread use of electrical stimulation may be limited by treatment protocols that increase operative time and complexity. This study evaluated whether a short-duration electrical stimulation protocol (10 minutes) was efficacious to enhance regeneration following nerve repair using rat models. METHODS: Lewis and Thy1-green fluorescent protein rats were randomized to three groups: 0 minutes of electrical stimulation (no electrical stimulation; control), 10 minutes of electrical stimulation, and 60 minutes of electrical stimulation. All groups underwent tibial nerve transection and repair. In the intervention groups, electrical stimulation was delivered after nerve repair. Outcomes were assessed using immunohistochemistry, histology, and serial walking track analysis. RESULTS: Two weeks after nerve repair, Thy1-green fluorescent protein rats demonstrated increased green fluorescent protein-positive axon outgrowth from the repair site with electrical stimulation compared to no electrical stimulation. Serial measurement of walking tracks after nerve repair revealed recovery was achieved more rapidly in both electrical stimulation groups as compared to no electrical stimulation. Histologic analysis of nerve distal to the repair at 8 weeks revealed robust axon regeneration in all groups. CONCLUSIONS: As little as 10 minutes of intraoperative electrical stimulation therapy increased early axon regeneration and facilitated functional recovery following nerve transection with repair. Also, as early axon outgrowth increased following electrical stimulation with nerve repair, these findings suggest electrical stimulation facilitated recovery because of earlier axon growth across the suture-repaired site into the distal nerve to reach end-organ targets. CLINICAL RELEVANCE STATEMENT: Brief (10-minute) electrical stimulation therapy can provide similar benefits to the 60-minute protocol in an acute sciatic nerve transection/repair rat model and merit further studies, as they represent a translational advantage.

Effect of Nimodipine and Botulinum Toxin A on Peripheral Nerve Regeneration in Rats: A Pilot Study.

BACKGROUND: Peripheral nerve damage is a frequent problem, with an estimated 2.8%-5.0% of trauma admissions involving peripheral nerve injury. End-to-end, tension-free microsurgical repair (neurorrhaphy) is the current gold standard treatment for complete transection (neurotmesis). While neurorrhaphy reapproximates the nerve, it does not address the complex molecular regenerative process. Evidence suggests that botulinum toxin A (BTX) and nimodipine (NDP) may improve functional recovery, but mechanisms of action remain unknown. METHODS: This research investigates BTX and NDP for their novel capacity to improve neural regeneration in the setting of neurorrhaphy using a Lewis rat tibial nerve neurotmesis model. In a triple-masked, placebo-controlled, randomized study design, we compared functional (rotarod, horizontal ladder walk), electrophysiological (conduction velocity, duration), and stereological (axon count, density) outcomes of rats treated with: NDP+saline injection, BTX+NDP, Saline+placebo, and BTX+placebo. Additional controls included sham surgery +/- BTX. RESULTS: NDP+saline outperformed other treatment groups in the ladder walk. This group had the fewest deep slips (15.07% versus 30.77% in BTX+NDP, P = 0.122), and the most correct steps (70.53% versus 55.58% in BTX+NDP, P = 0.149) in functional testing. NDP+saline also had the fastest nerve conduction velocity (0.811m/s versus 0.598m/s in BTX+NDP, P = 0.126) among treatment groups. BTX+NDP had the highest axon count (10,012.36 versus 7,738.18 in NDP+Saline, P = 0.009). CONCLUSION: This study is the first to test NDP with BTX in a multimodal assessment of nerve recovery following neurotmesis and neurorrhaphy. NDP outperformed BTX+NDP functionally. Future work will focus on nimodipine in an effort to improve nerve recovery in trauma patients.

Unrecognized tibial nerve injury in total-ankle arthroplasty: Two case reports.

RATIONALE: Tibial nerve injury is a sustainable but rare complication during total-ankle arthroplasty (TAA). We outlined 2 previously unreported cases of tibial nerve injury in TAA, including the prognoses and possible causes. PATIENT CONCERNS: First, a 63-year-old woman complained of a 5-month history of persistent tingling sensation and numbness on the medial and plantar aspects of her foot after TAA. Second, a 50-year-old woman complained of a 6-month history of tingling sensation and numbness on the plantar surface of her forefoot after TAA. DIAGNOSIS: Explorations were performed on suspicion of tarsal tunnel syndrome; however, both patients exhibited complete laceration of tibial nerve with neuroma formation. INTERVENTIONS: In both patients, we excised the neuroma and performed end-to-end nerve repair. OUTCOMES: The sensory disturbance of the sole considerably improved at long-term follow-up over 8 years after the neurorrhaphy procedures. LESSONS: Tibial nerve injury is rare following TAA, and is sometimes unrecognized or misdiagnosed. If tibial nerve injury is suspected, prompt surgical exploration should be performed; great precaution must also be taken to prevent injury of the tibial nerve during TAA.

Anatomical Considerations of Infrageniculate Popliteal Artery Puncture: Alternative Pathway for Retrograde Access After Failed Re-entry.

BACKGROUND: A distal approach in endovascular procedures for revascularization of lowers limbs can be considered in case of no re-entry in subintimal recanalization. The aim of this study is to evaluate the feasibility of a medial approach to the infrageniculate popliteal artery (IPA) using existing computed tomography (CT) scan simulation and punctures performed on cadavers. METHODS AND RESULTS: CT angiographies of lower extremities were used to simulate IPA puncture and puncture trajectory. Tissues damaged during the trajectory between the puncture site and the access-related injuries were analyzed. Anatomical punctures on cadaverous model were also performed. Corpses were placed in supine position, the hip in slight flexion (40°) and abduction (external rotation of 60°). A 16 G needle was used for the IPA puncture. Twelve CT angiography simulations were made. Of these 12 simulations, 9 revealed an isolated lesion of the popliteal vein and 2 isolated lesions of the tibial nerve. A lesion of the tibial nerve and the popliteal vein on the same simulation was once observed. Damage to the medial gastrocnemius muscle could not be avoided in each case. Ten punctures were performed on cadavers with technical success. There were 6 popliteal vein lesions, 3 tibial nerve lesions, and 1 case without lesion. In all cases, damage to the medial gastrocnemius muscle was seen. CONCLUSIONS: This medial approach was feasible and is accompanied by trauma of elements of the popliteal pedicle. Preoperative CT angiography could anticipate best site of puncture and potential access-related injury.

Schwannoma of the Posterior Tibial Nerve.

A 61-year-old woman was referred to physical therapy by a podiatrist who suspected a posterior tibialis degenerative tear. To further examine the irritable posterior tibial nerve, a musculoskeletal ultrasound examination was performed, showing a vascularized focal lesion suggestive of a nerve tumor. The patient was referred back to the referring podiatrist, who ordered magnetic resonance imaging, which confirmed the schwannoma of the posterior tibialis nerve. J Orthop Sports Phys Ther 2020;50(2):111. doi:10.2519/jospt.2020.9103.

Nerve Repair and Orthodromic and Antidromic Nerve Grafts: An Experimental Comparative Study in Rabbit.

PURPOSE: Although many surgeons have anecdotally described reversing the polarity of the autograft with the intent of improving regeneration, the optimal orientation of the autogenous nerve graft remains controversial. The aim of this study was to compare (1) the outcomes of orthodromic and antidromic nerve grafts to clarify the effect of nerve graft polarity and (2) the outcome of either form of nerve grafts with that of nerve repair. METHODS: In 14 of the 26 rabbits used in this study, a 1 cm defect was made in the tibial nerve. An orthodromic nerve graft on one side and an antidromic nerve graft on the other were performed using a 1.2 cm long segment of the peroneal nerve. In the remaining 12 rabbits, the tibial nerve was transected completely and then repaired microscopically on one side but left untreated on the other. Electrophysiologic studies were performed in all animals at 8 weeks after surgery, and the sciatic nerves were harvested. RESULTS: Compound motor action potential was visible in all rabbits treated by nerve repair but in only half of the rabbits treated by nerve graft. There was no significant difference in the compound motor action potential, nerve conduction velocity, or total number of axons between the orthodromic and antidromic nerve graft groups. However, in both groups, the outcome was significantly poorer than that of the nerve repair group. CONCLUSION: There was no significant difference by electromyographic or histologic evaluation between orthodromic and antidromic nerve grafts. Direct nerve repair with moderate tension may be a more effective treatment than nerve grafting.

Differential gene and protein expression in gastrocnemius and tibialis anterior muscle following tibial and peroneal nerve injury in rats.

Peripheral nerve injury is encountered quite commonly in the clinic, and treatment results are often not satisfactory. Therefore, promoting nerve regeneration and functional recovery is a primary goal of neuroscience research. Recovery of corresponding target muscle can differ following peripheral nerve injury, but the reasons are unknown. Herein, we investigated differential gene and protein expression in gastrocnemius and tibialis anterior muscle following tibial and common peroneal nerve injury using RNA sequencing and proteomics approaches, and analysed the results by bioinformatics. In total, 1794, 1765, 1656 and 2006 differential genes and 398, 400, 959 and 472 differential proteins were identified in gastrocnemius and tibialis anterior muscles at 1, 7, 14 and 21 days after surgery, related to activation of 51 signalling pathways. Differential expression of these genes and proteins may contribute to the degree of recovery of target organs following peripheral nerve injury. The findings provide a foundation for investigating regeneration mechanisms following peripheral nerve injury.

Conditioning electrical stimulation is superior to postoperative electrical stimulation, resulting in enhanced nerve regeneration and functional recovery.

Postoperative electrical stimulation (PES) improves nerve regeneration by decreasing staggered regeneration at the coaptation site. By contrast, conditioning (preoperative) electrical stimulation (CES) accelerates axon extension. Given that both techniques can be delivered at the bedside, a direct comparison of outcomes is of significant clinical importance. In this study, we compared regeneration and reinnervation outcomes of CES, PES, a combination of CES and PES, and a no stimulation control. Sprague Dawley rats were randomly divided into i) CES, ii) PES, iii) CES + PES, and iv) no stimulation. CES was delivered one week prior to nerve cut/coaptation, and PES was delivered immediately following nerve repair. Length of nerve regeneration was assessed at 7 days post-coaptation (n = 6/cohort), and behavioral testing was performed between 6 and 8 weeks post-coaptation (n = 8/cohort). Animals treated with CES had significantly longer axon extension and improved sensorimotor recovery compared to all other cohorts. CES treated axons extended 8.5 ± 0.6 mm, significantly longer than PES (5.5 ± 0.5 mm), CES + PES (3.6 ± 0.7 mm), or no stimulation (2.7 ± 0.5 mm) (p < .001). Sensory recovery (von Frey filament testing, intraepidermal nerve fiber reinnervation) (p < .001) and motor reinnervation (horizontal ladder, gait analysis, nerve conduction studies, neuromuscular junction analysis) (p < .05 - p < .001) were significantly improved in CES animals. CES significantly improves regeneration and reinnervation beyond the current clinical paradigm of PES. The combination of CES and PES does not have a synergistic effect. CES alone therefore may be a more promising treatment to improve outcomes in patients undergoing nerve repair surgeries.

Replantation and Lengthening of a Lower Leg in a 7-Year-Old Child: A Case Report.

Replantation of the lower leg has controversial indications, but it may be considered in carefully selected patients. Although the function of prosthetic lower legs has been improved in recent decades, leg salvage remains a laudable goal. We present the case of a 7-year-old child who sustained a traumatic amputation at the level of the middle tibia with loss of the middle portion of the lower leg. We performed successful replantation, and tibia lengthening was performed starting 10 days after replantation and lasted 6 months.

Effect of Reverse End-to-Side (Supercharging) Neurotization in Long Processed Acellular Nerve Allograft in a Rat Model.

PURPOSE: Processed acellular nerve allograft (PNA) has been suggested as a convenient tool for overcoming short and medium nerve defects. Although the clinical implications are unclear, animal data suggest that PNA becomes less effective at longer lengths. Although reverse or supercharging end-to-side nerve transfer may improve the neurotrophic potential in chronically denervated nerve tissue, the application of this strategy to long acellular nerve allograft has not been previously investigated. We hypothesized that supercharging acellular nerve allograft would increase its effective length. METHODS: Sprague-Dawley and Thy1-green fluorescent protein Sprague-Dawley rats underwent transection of the tibial nerve, followed by immediate repair with 20-, 40-, or 60-mm acellular nerve allografts processed identically to commercially available human acellular nerve allograft (AxoGen, Inc., Alachua, FL) or isograft. Half of the allograft group was supercharged with a reverse end-to-side transfer from the ipsilateral peroneal nerve. At 10 weeks, the reconstructed nerve in the Thy1-green fluorescent rat groups were exposed and examined under a fluorescence-enabled microscope. At 20 weeks, the remaining rats underwent motor testing and tissue harvest for morphological examination. RESULTS: In comparison with a nonenhanced allograft, supercharging had a statistically significant positive impact on the reinnervated muscle normalized force generation and distal axon counts for all graft sizes. Muscles in the supercharged group were heavier than those in the allograft group for the 40-mm-length grafts and G-ratio measurements were higher in the supercharged allograft group for 60-mm-length grafts only. CONCLUSIONS: This study supports that hypothesis that supercharging nerve transfer improves axon regeneration within PNA. CLINICAL RELEVANCE: When an appropriate donor nerve is available, supercharging nerve transfer may improve nerve regeneration in PNA across long nerve defects.

Ketamine reduces aversion in rodent pain models by suppressing hyperactivity of the anterior cingulate cortex.

Chronic pain is known to induce an amplified aversive reaction to peripheral nociceptive inputs. This enhanced affective response constitutes a key pathologic feature of chronic pain syndromes such as fibromyalgia. However, the neural mechanisms that underlie this important aspect of pain processing remain poorly understood, hindering the development of treatments. Here, we show that a single dose of ketamine can produce a persistent reduction in the aversive response to noxious stimuli in rodent chronic pain models, long after the termination of its anti-nociceptive effects. Furthermore, we demonstrated that this anti-aversive property is mediated by prolonged suppression of the hyperactivity of neurons in the anterior cingulate cortex (ACC), a brain region well known to regulate pain affect. Therefore, our results indicate that it is feasible to dissociate the affective from the sensory component of pain, and demonstrate the potential for low-dose ketamine to be an important therapy for chronic pain syndromes.

Management of an iatrogenic injury to the tibial nerve in a 24-year-old hurdle runner.

According to previously published papers, neurovascular injuries seem to be the most unfortunate complications after surgical procedures. In this report, we present our therapeutic approach to iatrogenic injury of the posterior tibial nerve that occurred during ankle arthroscopy in a 24-year-old patient. The outcome of the therapy was a full sensory return and partial motor return (S4 and M3 according to the Medical Research Council Grading System for Nerve Recovery). Our patient was able to resume her typical training. In comparison with available reports, our therapeutic approach enabled earlier functional recovery after nerve injury. While sensory return is beneficial, motor improvement is also important. However, we are conscious of the poor functional outcomes reported by other researchers.

Evaluation of different classes of histamine H1 and H2 receptor antagonist effects on neuropathic nociceptive behavior following tibial nerve transection in rats.

It seems that histamine release in the site of neuronal injury could contribute to the neuropathic pain mechanism. In the present study, we investigated the anti-allodynic effects of chronic administration of different classes of histamine H1 and H2 receptor antagonists on neuropathic nociceptive behavior following tibial nerve transection (TNT) in rats. Peripheral neuropathy was induced by TNT surgery. We performed acetone tests (AT) to record cold allodynia, Von Frey tests (VFT) to measure mechanical allodynia, double plate test (DPT) to evaluate thermal place preference/avoidance and open field test (OFT) for evaluation of animal activity. TNT rats showed a significant mechanical and cold allodynia compared to the sham group. Chlorpheniramine (5 and 15 mg/kg, i.p) significantly attenuated cold allodynia and prevented cold plate avoidance behavior and at the dose of 15 mg/kg remarkably decreased mechanical allodynia. Fexofenadine (10 and 30 mg/kg, p.o) significantly attenuated the mechanical allodynia and prevented cold plate avoidance. Ranitidine (5 and 15 mg/kg, i.p) significantly prevented cold plate avoidance behavior and at the dose of 15 mg/kg notably improved mechanical and cold allodynia. Famotidine (1 and 3 mg/kg, p.o) was ineffective on all nociceptive tests. Gabapantin (100 mg/kg, p.o) significantly improved all types of nociceptive behaviors. These results indicate that both blood brain barrier penetrating (chlorpheniramine) and poorly penetrating (fexofenadine) histamine H1 receptor antagonists could improve the neuropathic pain sign, but only the blood brain barrier penetrating histamine H2 receptor antagonist (ranitidine) could produce anti-allodynic effects in the TNT model of neuropathic pain in rats.

Botulinum Toxin Conditioning Enhances Motor Axon Regeneration in Mouse and Human Preclinical Models.

BACKGROUND: Peripheral axon regeneration is improved when the nerve lesion under consideration has recently been preceded by another nerve injury. This is known as the conditioning lesion effect (CLE). While the CLE is one of the most robust and well characterized means to enhance motor axon regeneration in experimental models, it is not considered a clinically feasible strategy. A pharmacological means to re-produce the CLE is highly desirable. OBJECTIVE: To test whether chemodenervation with a clinical grade formulation of botulinum toxin A (BoTX) would be sufficient to reproduce the CLE. METHODS: We examined the effects of a 1-week preconditioning administration of BoTX on motor axon regrowth in both a mouse tibial nerve injury and human embryonic stem cell (hESC)-based model. We assessed neuronal reinnervation in vivo (mice) with retrograde tracers and histological analysis of peripheral nerve tissue after injections into the triceps surae muscle group. We assessed motor neuron neurite outgrowth in vitro (hESC) after incubation in BoTX by immunohistochemistry and morphometric analysis. RESULTS: We found that BoTX conditioning treatment significantly enhanced outgrowth of both murine motor axons in vivo and human MN neurites in vitro. CONCLUSIONS: BoTX preconditioning represents a pharmacological candidate approach to enhance motor axon regeneration in specific clinical scenarios such as nerve transfer surgery. Further studies are needed to elucidate the molecular mechanism.

Rate of Neurologic Injury Following Lateralizing Calcaneal Osteotomy Performed Through a Medial Approach.

BACKGROUND: Calcaneal osteotomies are commonly used to correct varus hindfoot alignment in patients with symptomatic cavovarus deformity. Translational, closing wedge, and Malerba-type osteotomies have been implicated in the development of tarsal tunnel syndrome and neurologic injury to branches of the tibial nerve. The authors hypothesized that there would be minimal clinically important injury to the tibial nerve by performing a translational calcaneal osteotomy from a medial approach. METHODS: All patients undergoing a cavovarus reconstruction by a single surgeon were identified. Patients were included if they underwent a lateralizing calcaneal osteotomy via medial approach. Demographics, operative reports, and clinic notes were reviewed to identify concomitant procedures performed, incidence of postoperative tarsal tunnel syndrome, complications, and preoperative and postoperative nerve examinations. Postoperative radiographs were reviewed for location of the osteotomy relative to the posterior tubercle. RESULTS: Twenty-four patients underwent lateralizing calcaneal osteotomy via a medial approach. Of the osteotomies, 83.3% (20/24) were in the middle third of the calcaneus, with a mean of 11.6-mm translation. No patients developed postoperative tarsal tunnel syndrome or tibial nerve palsy. CONCLUSION: Lateralizing calcaneal osteotomy performed via a medial approach had a clinically negligible incidence of neurologic injury. Adequate translation was achieved to obtain correction of varus hindfoot deformity. The authors believe that there is less direct and less percussive injury to branches of the tibial nerve when performing the osteotomy from medial to lateral. This technique may represent an operative strategy to minimize risk to the tibial nerve and reduce neurologic deficit following cavovarus reconstruction. LEVEL OF EVIDENCE: Level IV, case series.