OBJECTIVE: To identify factors that contribute to iatrogenic sciatic nerve palsy during acetabular surgery through a Kocher-Langenbeck approach and to evaluate if variation among individual surgeons exists.
METHODS:
METHODS: Retrospective cohort.
METHODS: Level I trauma center.
UNASSIGNED: Adults undergoing fixation of acetabular fractures (AO/OTA 62) through a posterior approach by 9 orthopaedic traumatologists between November 2010 and November 2022.
UNASSIGNED: The prevalence of iatrogenic sciatic nerve palsy and comparison of the prevalence and risk of palsy between prone and lateral positions before and after adjusting for individual surgeon and the presence of transverse fracture patterns in logistic regression. Comparison of the prevalence of palsy between high-volume (>1 patient/month) and low-volume surgeons.
RESULTS: A total of 644 acetabular fractures repaired through a posterior approach were included (median age 39 years, 72% male). Twenty of 644 surgeries (3.1%) resulted in iatrogenic sciatic nerve palsy with no significant difference between the prone (3.1%, 95% confidence interval [CI], 1.9%-4.9%) and lateral (3.3%, 95% CI, 1.3%-8.1%) positions (P = 0.64). Logistic regression adjusting for surgeon and transverse fracture pattern demonstrated no significant effect for positions (odds ratio 1.0, 95% CI, 0.3-3.9). Transverse fracture pattern was associated with increased palsy risk (odds ratio 3.0, 95% CI, 1.1-7.9). Individual surgeon was significantly associated with iatrogenic palsy (P < 0.02).
CONCLUSIONS: Surgeon and the presence of a transverse fracture line predicted iatrogenic nerve palsy after a posterior approach to the acetabulum in this single-center cohort. Surgeons should perform the Kocher-Langenbeck approach for acetabular fixation in the position they deem most appropriate, as the position was not associated with the rate of iatrogenic palsy in this series.
METHODS: Prognostic Level III. See Instructions for Authors for a complete description of levels of evidence.

In the Old Testament book of Genesis, Chapter 32, Jacob wrestled with an angel. After that encounter, Jacobs limped. Through careful understanding of the original meaning of the words in Verses 25, 31, and 32 of Genesis 32, we seek to learn what type of injury the angel might have inflicted on Jacob. At the time Genesis was written, the difference between tendon and nerve was not understood. While wrestling, when the angel\'s hand grabbed Jacob, it was most likely Jacob\'s hip that was affected, not his thigh. Most likely, there was a posterior dislocation of the \"socket\" (hip joint), and the \"sinew\" that was damaged was the sciatic nerve. Today, this biblical description is manifested by the sciatic nerve being removed for beef to be considered Kosher. LAY SUMMARY: In Genesis Chapter 32, Jacob wrestled with an angel, after which Jacob limped. Most likely, Jacob had a posterior hip dislocation with a sciatic nerve stretch injury. Today, this Biblical description is manifested by the sciatic nerve being removed for beef to be considered Kosher.

Recent studies have shown that autophagy is activated in response to nerve damage and occurs simultaneously with the initial stages of Schwann cell-mediated demyelination. Although several studies have reported that macroautophagy is involved in the peripheral nerve, the role of chaperone-mediated autophagy (CMA) has not yet been investigated in peripheral nerve injury. The present study investigates the role of CMA in the sciatic nerve. Using a mouse model of sciatic nerve injury, the authors employed immunofluorescence analysis to observe the expression of LAMP2A, a critical marker for CMA. RNA sequencing was performed to observe the transcriptional profile of Lamp2a in Schwann cells. Bioinformatics analysis was carried out to observe the hub genes associated with Lamp2a . Expression of Lamp2a , a key gene in CMA, increased following sciatic nerve injury, based on an immunofluorescence assay. To identify differentially expressed genes using Lamp2a , RNA sequence analysis was conducted using rat Schwann cells overexpressing Lamp2a . The nine hub genes ( Snrpf, Polr1d, Snip1, Aqr, Polr2h, Ssbp1, Mterf3, Adcy6 , and Sbds ) were identified using the CytoHubba plugin of Cytoscape. Functional analysis revealed that Lamp2a overexpression affected the transcription levels of genes associated with mitotic spindle organization and mRNA splicing via the spliceosome. In addition, Polr1d and Snrpf1 were downregulated throughout postnatal development but elevated following sciatic nerve injury, according to a bioinformatics study. CMA may be an integral pathway in sciatic nerve injury via mRNA splicing.

BACKGROUND: While sciatic nerve injury has been described as a complication of acetabular fractures, iatrogenic nerve injury remains sparsely reported. This study aims to assess iatrogenic sciatic nerve injuries occurring during acetabular fracture surgery, tracking their neurological recovery and clinical outcomes, and investigating any correlation between recovery and the severity of neurologic injury to facilitate physicians in providing prediction of prognosis.
METHODS: We present two cases of male patients, aged 56 and 22, who developed sciatic palsy due to iatrogenic nerve injury during acetabular fracture surgery. Iatrogenic sciatic nerve injury resulted from operatively treated acetabular fractures. Surgical exploration, involving internal fixation removal and nerve decompression, successfully alleviated symptoms in both cases postoperatively. At the latest follow-up, one patient achieved full recovery with excellent function, while the other exhibited residual deficits at the L5/S1 root level along with minimal pain.
CONCLUSIONS: Sciatic nerve injury likely stemmed from reduction techniques and internal fixation procedures for the posterior column, particularly when performed with the hip flexed, thereby placing tension on the sciatic nerve. Our case reports underscore the significance of liberal utilization of electrophysiologic examinations and intraoperative monitoring for the prediction of prognosis. Surgical exploration, encompassing internal fixation removal and nerve decompression, represents an effective intervention for resolving sciatic palsy, encompassing both sensory neuropathy and motor symptoms.

Peripheral nerves exhibit long-term residual motor dysfunction following injury. The length of the denervation period before nerve and muscle reconnection is an important factor in motor function recovery. We aimed to investigate whether repeated nerve crush injuries to the same site every 7 days would preserve the conditioning lesion (CL) response and to determine the number of nerve crush injuries required to create an experimental animal model that would prolong the denervation period while maintaining peripheral nerve continuity. Rats were grouped according to the number of sciatic nerve crushes. A significant decrease in the soleus muscle fiber cross-sectional area was observed with increased crushes. After a single crush, macrophage accumulation and macrophage chemotaxis factor CCL2 expression in dorsal root ganglia were markedly increased, which aligned with the gene expression of Ccl2 and its receptor Ccr2. Macrophage numbers, histological CCL2 expression, and Ccl2 and Ccr2 gene expression levels decreased, depending on the number of repeated crushes. Histological analysis and gene expression analysis in the group with four repeated crushes did not differ significantly when compared with uninjured animals. Our findings indicated that repeated nerve crushes at the same site every 7 days sustained innervation loss and caused a loss of the CL response. The experimental model did not require nerve stump suturing and is useful for exploring factors causing prolonged denervation-induced motor dysfunction. SIGNIFICANCE STATEMENT: This study elucidates the effects of repeated nerve crush injury to the same site on innervation and conditioning lesion responses and demonstrates the utility of an experimental animal model that recapitulates the persistent residual motor deficits owing to prolonged denervation without requiring nerve transection and transection suturing.

BACKGROUND: Since the 1990s, evidence has accumulated that macrophages promote peripheral nerve regeneration and are required for enhancing regeneration in the conditioning lesion (CL) response. After a sciatic nerve injury, macrophages accumulate in the injury site, the nerve distal to that site, and the axotomized dorsal root ganglia (DRGs). In the peripheral nervous system, as in other tissues, the macrophage response is derived from both resident macrophages and recruited monocyte-derived macrophages (MDMs). Unresolved questions are: at which sites do macrophages enhance nerve regeneration, and is a particular population needed.
METHODS: Ccr2 knock-out (KO) and Ccr2gfp/gfp knock-in/KO mice were used to prevent MDM recruitment. Using these strains in a sciatic CL paradigm, we examined the necessity of MDMs and residents for CL-enhanced regeneration in vivo and characterized injury-induced nerve inflammation. CL paradigm variants, including the addition of pharmacological macrophage depletion methods, tested the role of various macrophage populations in initiating or sustaining the CL response. In vivo regeneration, measured from bilateral proximal test lesions (TLs) after 2 d, and macrophages were quantified by immunofluorescent staining.
RESULTS: Peripheral CL-enhanced regeneration was equivalent between crush and transection CLs and was sustained for 28 days in both Ccr2 KO and WT mice despite MDM depletion. Similarly, the central CL response measured in dorsal roots was unchanged in Ccr2 KO mice. Macrophages at both the TL and CL, but not between them, stained for the pro-regenerative marker, arginase 1. TL macrophages were primarily CCR2-dependent MDMs and nearly absent in Ccr2 KO and Ccr2gfp/gfp KO mice. However, there were only slightly fewer Arg1+ macrophages in CCR2 null CLs than controls due to resident macrophage compensation. Zymosan injection into an intact WT sciatic nerve recruited Arg1+ macrophages but did not enhance regeneration. Finally, clodronate injection into Ccr2gfp KO CLs dramatically reduced CL macrophages. Combined with the Ccr2gfp KO background, depleting MDMs and TL macrophages, and a transection CL, physically removing the distal nerve environment, nearly all macrophages in the nerve were removed, yet CL-enhanced regeneration was not impaired.
CONCLUSIONS: Macrophages in the sciatic nerve are neither necessary nor sufficient to produce a CL response.

OBJECTIVE: As a first step towards developing a core outcome set (COS) for sciatic neuropathy, the goal of the current study was to perform a systematic review of the literature to identify outcome measures that have been previously reported in studies on sciatic neuropathy.
METHODS: A systematic review of the literature from 2000-2024 was performed utilizing PubMed and Medical Subject Headings (MeSH). Identified articles were screened according to study inclusion/exclusion criteria. Outcome measures reported in each included study were recorded and categorized into motor, sensory, pain, patient-reported outcomes, electrodiagnostic outcomes, imaging outcomes, and composite outcomes. Descriptive statistics were performed.
RESULTS: A total of 1586 articles were initially identified, and 31 articles met criteria for inclusion and underwent analysis. The most common outcome domain was pain. A pain outcome was reported in 17 (63%) studies. A motor outcome was reported in 10 (37%) studies; 6 (22%) reported a sensory outcome; 1 (4%) reported a composite outcome; 4 (15%) reported an electrodiagnostic outcome; 5 (19%) reported a patient-reported outcome; 3 (11%) reported an imaging outcome. Across the included studies, 21 unique outcomes were reported.
CONCLUSIONS: We have identified the outcome measures that have previously been utilized in studies on sciatic neuropathy. Previously used outcome measures fell into seven domains: motor outcomes, sensory outcomes, pain outcomes, patient-reported outcomes, electrodiagnostic outcomes, imaging outcomes, and composite outcomes. Pain outcomes were most commonly used across the included studies.

BACKGROUND: Despite the high prevalence of neuropathic pain, treating this neurological disease remains challenging, given the limited efficacy and numerous side effects associated with current therapies. The complexity in patient management is largely attributed to an incomplete understanding of the underlying pathological mechanisms. Central sensitization, that refers to the adaptation of the central nervous system to persistent inflammation and heightened excitatory transmission within pain pathways, stands as a significant contributor to persistent pain. Considering the role of the cystine/glutamate exchanger (also designated as system xc-) in modulating glutamate transmission and in supporting neuroinflammatory responses, we investigated the contribution of this exchanger in the development of neuropathic pain.
METHODS: We examined the implication of system xc- by evaluating changes in the expression/activity of this exchanger in the dorsal spinal cord of mice after unilateral partial sciatic nerve ligation. In this surgical model of neuropathic pain, we also examined the consequence of the genetic suppression of system xc- (using mice lacking the system xc- specific subunit xCT) or its pharmacological manipulation (using the pharmacological inhibitor sulfasalazine) on the pain-associated behavioral responses. Finally, we assessed the glial activation and the inflammatory response in the spinal cord by measuring mRNA and protein levels of GFAP and selected M1 and M2 microglial markers.
RESULTS: The sciatic nerve lesion was found to upregulate system xc- at the spinal level. The genetic deletion of xCT attenuated both the amplitude and the duration of the pain sensitization after nerve surgery, as evidenced by reduced responses to mechanical and thermal stimuli, and this was accompanied by reduced glial activation. Consistently, pharmacological inhibition of system xc- had an analgesic effect in lesioned mice.
CONCLUSIONS: Together, these observations provide evidence for a role of system xc- in the biochemical processes underlying central sensitization. We propose that the reduced hypersensitivity observed in the transgenic mice lacking xCT or in sulfasalazine-treated mice is mediated by a reduced gliosis in the lumbar spinal cord and/or a shift in microglial M1/M2 polarization towards an anti-inflammatory phenotype in the absence of system xc-. These findings suggest that drugs targeting system xc- could contribute to prevent or reduce neuropathic pain.

Piriformis syndrome is a condition that is proposed to result from compression of the sciatic nerve, either in whole or in part, in the deep gluteal space by the piriformis muscle. The prevalence of piriformis syndrome depends upon the diagnostic criteria being used and the population studied but is estimated by some to be 5%-6% in all cases of low back, buttock, and leg pain and up to 17% of patients with chronic low back pain. While the sciatic nerve may pierce the piriformis muscle in about 16% of healthy individuals, this frequency is no different in those with the syndrome; thus, the relationship to this anatomic finding is unclear. The most common symptoms are buttock pain, external tenderness over the greater sciatic notch, and aggravation of the pain through sitting. Many clinical signs are reported for piriformis syndrome, but the sensitivity and specificity are unclear, in part because of the lack of a uniformly accepted case definition. In the majority of cases in the literature, it appears that the diagnosis is more ascribed to a myofascial condition rather than a focal neuropathy. Electrodiagnostic studies can be useful to exclude other causes of symptoms, but there is no well-accepted test to confirm the presence of piriformis syndrome. Ultrasound imaging may show thickening of the piriformis muscle, but further research is required to confirm that this is correlated with the clinical diagnosis. Magnetic resonance imaging and neurography may hold promise in the future, but there are not yet sufficient data to support adopting these methods as a standard diagnostic tool. The initial treatment of piriformis syndrome is typically conservative management with the general rehabilitation principles similar to other soft tissue musculoskeletal conditions. Local anesthetic, botulinum toxin, and/or corticosteroid injections have been reported by some to be beneficial for diagnostic or treatment purposes. Surgical interventions have also been used with variable success.

The sciatic nerve is the body\'s largest peripheral nerve. Along with their two terminal divisions (tibial and fibular), their anatomic location makes them particularly vulnerable to trauma and iatrogenic injuries. A thorough understanding of the functional anatomy is required to adequately localize lesions in this lengthy neural pathway. Proximal disorders of the nerve can be challenging to precisely localize among a range of possibilities including lumbosacral pathology, radiculopathy, or piriformis syndrome. A correct diagnosis is based upon a thorough history and physical examination, which will then appropriately direct adjunctive investigations such as imaging and electrodiagnostic testing. Disorders of the sciatic nerve and its terminal branches are disabling for patients, and expert assessment by rehabilitation professionals is important in limiting their impact. Applying techniques established in the upper extremity, surgical reconstruction of lower extremity nerve dysfunction is rapidly improving and evolving. These new techniques, such as nerve transfers, require electrodiagnostic assessment of both the injured nerve(s) as well as healthy, potential donor nerves as part of a complete neurophysiological examination.