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Background. The purpose of this prospective, double-blinded randomized control pilot study was to evaluate the effect of adjunctive dexamethasone on analgesia duration and the incidence of postoperative neuropathic complication. Peripheral nerve blocks are an effective adjunct to decrease postoperative pain in foot and ankle surgery, and any possible modalities to augment their efficacy is of clinical utility. Methods. Patients were randomly assigned to a control group (n = 25) receiving nerve blocks of bupivacaine and epinephrine or an experimental group (n = 24) with an adjunctive 8 mg dexamethasone. The patients, surgeons, and anesthesiologists were all blinded to allocation. Patients had a minimum 1 year postoperative follow-up. Results. Forty-nine patients completed the protocol. There was no statistically significant difference in analgesia duration (P = .38) or postoperative neuropathic complication incidence (P = .67) between the 2 groups. Conclusions. The addition of dexamethasone to popliteal nerve blocks does not appear to affect analgesia duration or incidence of postoperative neuropathic complications. However, our study was underpowered, and we recommend a larger scale prospective study for validation.Levels of Evidence: Level II: Prospective, randomized control pilot study.

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A 39-year-old man presented with an 8-month history of pain and paresthesia of the right foot sole and difficulty in the right toe dorsiflexion. A neurological examination revealed weakness in performing both the ankle and right foot toe dorsiflexion, reduced right planta pedis sensation, and absent right Achilles tendon reflex. Tinel's sign was present on the right popliteal fossa and medial part of the right ankle. MRI of the right knee showed multiple cystic lesions in his right tibial nerve. The cystic lesions extended from the popliteal fossa and were thought to be intraneural ganglion cysts. On MRI performed 4 months later, most of the cystic lesions spontaneously vanished. Therefore, intraneural ganglia should be considered when atypical mononeuropathy, such as tibial nerve palsy, is present.

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OBJECTIVE: Determine the incidence of tibial neuropathy following talus fractures and CT's ability to stratify patients at risk for developing post-traumatic neuropathy. MATERIALS AND METHODS: In this IRB-approved retrospective analysis, 71 talus fractures and 8 contralateral control ankle CTs were reviewed by one observer blinded to clinical information. CT evidence suggestive of tibial neurovascular bundle injury included nerve displacement, perineural fat effacement/edema, and bone touching nerve. The association between these CT findings and clinically evident tibial neuropathy was analyzed. A semi-quantitative likelihood score was assigned based on the degree of the CT findings around the nerve. Interobserver agreement was calculated between 2 other readers. RESULTS: Twenty-five percent of patients in this cohort had clinical evidence of tibial neuropathy. There was a high specificity (0.87-0.93) and negative predictive value (0.83-0.87), a moderate accuracy (0.80-0.82), but a lower sensitivity (0.33-0.56) associated with the CT findings. Among the CT findings, nerve displacement (p < 0.0001) and bone touching nerve (p = 0.01) were associated with tibial neuropathy. A likelihood score of 2-5 was associated (p = 0.007-0.015) with tibial neuropathy. The presence of tibial neuropathy and nerve recovery were not associated with hospital length of stay, while CT findings were. There was substantial agreement between the three readers: likelihood scores 2+ (k = 0.78) and 3+ (k = 0.72). CONCLUSIONS: Tibial neuropathy occurs following talus fractures, and CT findings may help surgeons narrow down the number of patients requiring close neurological follow-up.

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A case report of traumatic neuroma, a benign non-neoplastic tumor of the posterior tibial nerve is presented. The soft tissue mass in the midfoot region was likely a sequela of previous nerve decompression surgery that the patient underwent five years previously in the same region and on the same nerve. Physical examination and history taking, along with an MRI, were important steps in reaching a definitive diagnosis of traumatic neuroma based on the findings of an interventional radiologist and histopathological evaluation of the biopsy by a pathologist. The lesion was subsequently surgically removed utilizing a multidisciplinary management approach. The patient recovered uneventfully and no symptom recurrence was noted at the 30-month follow-up. The tumor was the largest reported in the literature at the time. This case was also unique in that the patient was relieved of pronation and regained tactile sensation in the midfoot.

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Ischemic neuropathy is an exceedingly rare complication after peripheral artery embolization. We report a case of ischemic damage to the tibial and peroneal nerve after embolization of the vasa nervorum that served as feeding collaterals to a surgically excluded popliteal artery aneurysm.

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Background: Lateralizing calcaneal osteotomy (LCO) is a common procedure used to correct hindfoot varus. Several complications have been described in the literature, but only a few articles describe tibial nerve palsy after this procedure. Our hypothesis was that tibial nerve palsy is a common complication after LCO. Methods: A retrospective study of patients undergoing LCO for hindfoot varus between 2007 and 2013 was performed. A total of 15 patients (18 feet) were included in the study. The patients were examined for tibial nerve deficit, and all the patients were examined with a computed tomography (CT) scan of both feet. Patients with a preexisting neurological disease were excluded. The primary outcome was tibial nerve palsy, and the secondary outcomes were reduction of the tarsal tunnel volume, the distance from subtalar joint to the osteotomy, and the lateral step at the osteotomy evaluated by CT scans. Results: Three of the 18 feet examined had tibial nerve palsy at a mean follow-up of 51 months. The mean reduction in tarsal tunnel volume when comparing the contralateral nonoperated foot to the foot operated with LCO was 2732 mm3 in the group without neurological deficit and 2152 mm3 in the group with neurological deficit (P = .60). Conclusion: 3 of 18 feet had tibial palsy as a complication to LCO. We were not able to show that a larger decrease in the tarsal tunnel volume, a more anterior calcaneal osteotomy, or a larger lateral shift of the osteotomy is associated with tibial nerve palsy. Levels of Evidence: Level IV: Retrospective case series.

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Intraneural electrodes must be in intimate contact with nerve fibers to have a proper function, but this interface is compromised due to the foreign body reaction (FBR). The FBR is characterized by a first inflammatory phase followed by a second anti-inflammatory and fibrotic phase, which results in the formation of a tissue capsule around the implant, causing physical separation between the active sites of the electrode and the nerve fibers. We have tested systemically several anti-inflammatory drugs such as dexamethasone (subcutaneous), ibuprofen and maraviroc (oral) to reduce macrophage activation, as well as clodronate liposomes (intraperitoneal) to reduce monocyte/macrophage infiltration, and sildenafil (oral) as an antifibrotic drug to reduce collagen deposition in an FBR model with longitudinal Parylene C intraneural implants in the rat sciatic nerve. Treatment with dexamethasone, ibuprofen, or clodronate significantly reduced the inflammatory reaction in the nerve in comparison to the saline group after 2 weeks of the implant, whereas sildenafil and maraviroc had no effect on infiltration of macrophages in the nerve. However, only dexamethasone was able to significantly reduce the matrix deposition around the implant. Similar positive results were obtained with dexamethasone in the case of polyimide-based intraneural implants, another polymer substrate for the electrode. These results indicate that inflammation triggers the FBR in peripheral nerves, and that anti-inflammatory treatment with dexamethasone may have beneficial effects on lengthening intraneural interface functionality. Anat Rec, 301:1722-1733, 2018. © 2018 Wiley Periodicals, Inc.

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We report the first case of distal posterior tibial nerve injury after arthroscopic calcaneoplasty. A 59-year-old male had undergone right arthroscopic calcaneoplasty to treat retrocalcaneal bursitis secondary to a Haglund's deformity. The patient complained of numbness in his right foot immediately after the procedure. Two years later and after numerous assessments and investigations, a lateral plantar nerve and medial calcaneal nerve lesion was diagnosed. In the operating room, the presence of an iatrogenic lesion to the distal right lateral plantar nerve (neuroma incontinuity involving 20% of the nerve) and the medial calcaneal nerve (complete avulsion) was confirmed. The tarsal tunnel was decompressed, and both the medial and the lateral plantar nerve were neurolyzed under magnification. To the best of our knowledge, our case report is the first to describe iatrogenic posterior tibial nerve injury after arthroscopic calcaneoplasty. It is significant because this complication can hopefully be avoided in the future with careful planning and creation of arthroscopic ports and treated appropriately with early referral to a nerve specialist if the patient's symptoms do not improve within 3 months.

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BACKGROUND: Lateralizing calcaneal osteotomy (LCO) is a frequently used technique to correct hindfoot varus deformity. Tibial nerve palsy following this osteotomy has been described in case reports but the incidence has not been quantified. METHODS: Eighty feet in 72 patients with cavovarus foot deformity were treated over a 6-year span by 2 surgeons at their respective institutions. Variations of the LCO were employed for correction per surgeon choice. A retrospective chart review analyzed osteotomy type, osteotomy location, amount of translation, and addition of a tarsal tunnel release in relation to the presence of any postoperative tibial nerve palsy. Tibial nerve branches affected and the time to resolution of any deficits was also noted. RESULTS: The incidence of neurologic deficit following LCO was 34%. With an average follow-up of 19 months, a majority (59%) resolved fully at an average of 3 months. There was a correlation between the development of neurologic deficit and the location of the osteotomy in the middle third as compared to the posterior third of the calcaneal tuber. We found no relationship between the osteotomy type, amount of correction, or addition of a tarsal tunnel release and the incidence of neurologic injury. CONCLUSIONS: Tibial nerve palsy was not uncommon following LCO. Despite the fact that deficits were found to be transient, physicians should be more aware of this potential problem and counsel patients accordingly. To decrease the risk of this complication, we advocate extra caution when performing the osteotomy in the middle one-third of the calcaneal tuberosity. Although intuitively the addition of a tarsal tunnel release may protect against injury, no protective effect was demonstrated in this retrospective study. LEVEL OF EVIDENCE: Level III, retrospective cohort study.

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We present a case of tibial nerve impingement by an anteroposterior screw inserted for stabilization of a posterior malleolar fracture. This specific complication has not previously been described in published studies, although numerous reports have described various forms of peripheral nerve entrapment. We discuss the merits of fixation of these fractures using a posterolateral approach.

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OBJECT Knee dislocations are often accompanied by stretch injuries to the common peroneal nerve (CPN). A small subset of these injuries also affect the tibial nerve. The mechanism of this combined pattern could be a single longitudinal stretch injury of the CPN extending to the sciatic bifurcation (and tibial division) or separate injuries of both the CPN and tibial nerve, either at the level of the tibiofemoral joint or distally at the soleal sling and fibular neck. The authors reviewed cases involving patients with knee dislocations with CPN and tibial nerve injuries to determine the localization of the combined injury and correlation between degree of MRI appearance and clinical severity of nerve injury. METHODS Three groups of cases were reviewed. Group 1 consisted of knee dislocations with clinical evidence of nerve injury (n = 28, including 19 cases of complete CPN injury); Group 2 consisted of knee dislocations without clinical evidence of nerve injury (n = 19); and Group 3 consisted of cases of minor knee trauma but without knee dislocation (n = 14). All patients had an MRI study of the knee performed within 3 months of injury. MRI appearance of tibial and common peroneal nerve injury was scored by 2 independent radiologists in 3 zones (Zone I, sciatic bifurcation; Zone II, knee joint; and Zone III, soleal sling and fibular neck) on a severity scale of 1-4. Injury signal was scored as diffuse or focal for each nerve in each of the 3 zones. A clinical score was also calculated based on Medical Research Council scores for strength in the tibial and peroneal nerve distributions, combined with electrophysiological data, when available, and correlated with the MRI injury score. RESULTS Nearly all of the nerve segments visualized in Groups 1 and 2 demonstrated some degree of injury on MRI (95%), compared with 12% of nerve segments in Group 3. MRI nerve injury scores were significantly more severe in Group 1 relative to Group 2 (2.06 vs 1.24, p < 0.001) and Group 2 relative to Group 3 (1.24 vs 0.13, p < 0.001). In both groups of patients with knee dislocations (Groups 1 and 2), the MRI nerve injury score was significantly higher for CPN than tibial nerve (2.72 vs 1.40 for Group 1, p < 0.001; 1.39 vs 1.09 for Group 2, p < 0.05). The clinical injury score had a significantly strong correlation with the MRI injury score for the CPN (r = 0.75, p < 0.001), but not for the tibial nerve (r = 0.07, p = 0.83). CONCLUSIONS MRI is highly sensitive in detecting subclinical nerve injury. In knee dislocation, clinical tibial nerve injury is always associated with simultaneous CPN injury, but tibial nerve function is never worse than peroneal nerve function. The point of maximum injury can occur in any of 3 zones.

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Proximal tibial neuropathy is an uncommon focal mononeuropathy that is most often caused by trauma, ischemia, or neoplastic infiltration or compression of the tibial nerve. We report a patient who presented with a tibial neuropathy following a leg injury, which initially mimicked a lumbosacral radiculopathy but which was the result of a proximal tibial neuropathy. Electrophysiologic studies confirmed a proximal tibial neuropathy and MRI revealed a popliteus muscle hemorrhage with mass effect on the tibial nerve. Following conservative management the patient had little recovery of function after 15 months.

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PURPOSE: This article reports on nine cases of proximal tibial nerve compression by the soleal tendinous arch caused by unsuitable treatment of acute compartment syndrome (ACS). Also, we report the clinical results of neurolysis and analyse the cause of this special type of neurological compression. METHODS: There were nine extremities in nine patients included in the study. All patients were among the victims of the Wenchuan earthquake in 2008. All patients had a previous lower extremity ACS. Pain level, numbness in the sole, muscle strength of the flexor hallucis longus and Tinel's sign were evaluated pre- and post-operatively. Each proximal tibial nerve compression was subjected to neurolysis with division of the soleal tendinous arch. RESULTS: At a mean follow-up of 22 months, eight patients (87 %) with weakness of the flexor hallucis longus showed improvement in flexor strength and seven patients (78 %) exhibited improved sensory function in the sole. All patients experienced pain relief. Subjective pain was reduced from an average score of 2.7 to 0.7 based on a visual analogue scale. Physical examination for Tinel's sign revealed all patients experienced relief of radiating pain, but two patients still retained a positive Tinel's sign (mild) over the soleal tendinous arch. In summary, four patients were highly satisfied, four were satisfied and one was neither satisfied nor dissatisfied with functional recovery after neurolysis. CONCLUSIONS: Unsuitable treatment of lower extremity ACS can lead to tibial nerve compression beneath the soleal tendinous arch. Neurolysis may improve pain and sensory and motor function.

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