Injured Nerve Research Articles

Activation of TGR5 in the injured nerve site according to a prevention protocol mitigates partial sciatic nerve ligation-induced neuropathic pain by alleviating neuroinflammation.

Neuropathic pain is a pervasive medical challenge currently lacking effective treatment options. Molecular changes at the site of peripheral nerve injury contribute to both peripheral and central sensitization, critical components of neuropathic pain. This study explores the role of the G-protein-coupled bile acid receptor (GPBAR1 or TGR5) in the peripheral mechanisms underlying neuropathic pain induced by partial sciatic nerve ligation in male mice. TGR5 was upregulated in the injured nerve site and predominantly colocalized with macrophages. Perisciatic nerve administration of the TGR5 agonist, INT-777 according to a prevention protocol (50 μg/μL daily from postoperative day [POD] 0 to POD6) provided sustained relief from mechanical allodynia and spontaneous pain, whereas the TGR5 antagonist, SBI-115 worsened neuropathic pain. Transcriptome sequencing linked the pain relief induced by TGR5 activation to reduced neuroinflammation, which was further evidenced by a decrease in myeloid cells and pro-inflammatory mediators (eg, CCL3, CXCL9, interleukin [IL]-6, and tumor necrosis factor [TNF] α) and an increase in CD86-CD206+ anti-inflammatory macrophages at POD7. Besides, myeloid-cell-specific TGR5 knockdown in the injured nerve site exacerbated both neuropathic pain and neuroinflammation, which was substantiated by bulk RNA-sequencing and upregulated expression levels of inflammatory mediators (including CCL3, CCL2, IL-6, TNF α, and IL-1β) and the increased number of monocytes/macrophages at POD7. Furthermore, the activation of microglia in the spinal cord on POD7 and POD14 was altered when TGR5 in the sciatic nerve was manipulated. Collectively, TGR5 activation in the injured nerve site mitigates neuropathic pain by reducing neuroinflammation, while TGR5 knockdown in myeloid cells worsens pain by enhancing neuroinflammation.

Thyroid Radiofrequency Ablation-Thermal Effects on Recurrent Laryngeal Nerve Using Continuous Intraoperative Neuromonitoring Animal Model.

When performing radiofrequency ablation for thyroid nodules, it is essential to avoid thermal injury to the recurrent laryngeal nerve. This porcine animal model study used continuous intraoperative neuromonitoring to investigate the thermal safety parameters of thyroid radiofrequency ablation. Porcine animal study. University animal laboratory. Twelve piglets were tested at different radiofrequency power levels, and the real-time electromyography signal changes were recorded under continuous intraoperative neuromonitoring. The spread heat study (8 piglets) included spontaneous recovery tests and cold water irrigation tests to investigate the safety distance from the recurrent laryngeal nerve to the active tip during 5-second activation with standard stimulation patterns. The residual heat study (4 piglets) investigated the safety cooling durations by touching the recurrent laryngeal nerve with the tip after a 5-second activation. In the spread heat study, substantial signal attenuation events were observed at an spread heat distance of 2, 3, 5, and 5 mm when the power was set as 10, 20, 30, and 50 W, respectively. No signal recovery could be observed in 20 minutes with or without cold water irrigation in the injured recurrent laryngeal nerve area. The residual heat study shows the residual thermal effect of the tip is minimal, and no substantial signal attenuation event was observed at all experiments. This innovative study established the thermal safety parameters for radiofrequency ablation in a porcine model at various power levels, which can potentially assist operators in delineating a precise ablation field and providing effective thyroid ablation treatment safely.

Fabrication and characterization of bioresorbable, electroactive and highly regular nanomodulated cell interfaces

Biomaterial-based implantable scaffolds capable of promoting physical and functional reconnection of injured spinal cord and nerves represent the latest frontier in neural tissue engineering. Here, we report the fabrication and characterization of self-standing, biocompatible and bioresorbable substrates endowed with both controlled nanotopography and electroactivity, intended for the design of transient implantable scaffolds for neural tissue engineering. In particular, we obtain conductive and nano-modulated poly(D,L-lactic acid) (PLA) and poly(lactic-co-glycolic acid) free-standing films by simply iterating a replica moulding process and coating the polymer with a thin layer of poly(3,4-ethylendioxythiophene) polystyrene sulfonate. The capability of the substrates to retain both surface patterning and electrical properties when exposed to a liquid environment has been evaluated by atomic force microscopy, electrochemical impedance spectroscopy and thermal characterizations. In particular, we show that PLA-based films maintain their surface nano-modulation for up to three weeks of exposure to a liquid environment, a time sufficient for promoting axonal anisotropic sprouting and growth during neuronal cell differentiation. In conclusion, the developed substrates represent a novel and easily-tunable platform to design bioresorbable implantable devices featuring both topographic and electrical cues.

Peripheral nerve grafting

Peripheral nerve lesions often lead to significant and permanent loss of motor and sensory function. The aim of peripheral nerve grafting is to bridge nerve defects. When tension-free nerve repair is not possible, peripheral nerve grafting is indicated. Local infection, insufficient soft tissue coverage, significant muscle atrophy or joint contraction in case of "motor" nerve grafting, lack of microsurgical instruments or experience, life-threatening injuries. Exposure and preparation of the nerve stumps. Choosing and preparation of the donor nerve. Approximation. Nerve repair. Nerve reconstruction must always be tension-free as nerve repair with tension frequently leads to disruption of nerve healing and poor functional outcome. Autologous nerve grafting from various donor sites leads to excellent functional results with little sensory deficits at the donor regions. Limited immobilization, physiotherapy, ergotherapy, regular clinical and neurological assessments. Outcome of peripheral nerve grafting may, for example, depend on defect length, caliber and quality of the injured nerve, quality of the donor nerve, microsurgical expertise of the surgeon, time of reconstruction, and age of the patient.

Single-cell profiling of cellular changes in the somatic peripheral nerves following nerve injury.

Injury to the peripheral nervous system disconnects targets to the central nervous system, disrupts signal transmission, and results in functional disability. Although surgical and therapeutic treatments improve nerve regeneration, it is generally hard to achieve fully functional recovery after severe peripheral nerve injury. A better understanding of pathological changes after peripheral nerve injury helps the development of promising treatments for nerve regeneration. Single-cell analyses of the peripheral nervous system under physiological and injury conditions define the diversity of cells in peripheral nerves and reveal cell-specific injury responses. Herein, we review recent findings on the single-cell transcriptome status in the dorsal root ganglia and peripheral nerves following peripheral nerve injury, identify the cell heterogeneity of peripheral nerves, and delineate changes in injured peripheral nerves, especially molecular changes in neurons, glial cells, and immune cells. Cell-cell interactions in peripheral nerves are also characterized based on ligand-receptor pairs from coordinated gene expressions. The understanding of cellular changes following peripheral nerve injury at a single-cell resolution offers a comprehensive and insightful view for the peripheral nerve repair process, provides an important basis for the exploration of the key regulators of neuronal growth and microenvironment reconstruction, and benefits the development of novel therapeutic drugs for the treatment of peripheral nerve injury.

The long-term functional outcome of the mangled upper extremity intricate management. A single center experience

PurposeSevere injury of multiple anatomical structures of the upper extremity can be caused by an extremely violent mechanism during labor and motor vehicle accidents, gunshots and explosions. The mangled upper extremity consists of trauma of at least 3 of 4 tissue types: connective tissue (skin, subcutaneous tissue, tendons, muscles), vessels, nerves, and bones. The purpose of this study is to evaluate the medium and long-term results of the limb salvage management of those injuries in our department. MethodsSixty-seven patients with multi-injured upper limb were operated in our department between 2014 and 2022 and evaluated with clinical examination and questionnaires (PROMs) on an outpatient basis at a mean follow up of 7.4 years. Patients’ demographics, the injured anatomic structures and the surgical interventions needed, were recorded. ResultsThe overall outcome, configured by functional scores was quite acceptable concerning injuries’ severity. Nineteen patients (29 %) underwent more than one operation, 2-point discrimination test was impaired in 30 % of the patients who had an injured nerve and total loss of regional sensation was diagnosed in 2 patients. Primary amputation was necessary in 8 % of the patients. ConclusionsEven though the mangled upper extremity refers to a severe injury with often poor postoperative results and high rates of amputations, a thorough evaluation and management by expert hand surgeons is essential for maximizing the possible outcomes.

Schwann cell-secreted frizzled-related protein 1 dictates neuroinflammation and peripheral nerve degeneration after neurotrauma.

Neurotrauma in limbs can induce sustained neuroinflammation, resulting in persistent disruption of nerve tissue architecture and retardation of axon regrowth. Despite macrophage-mediated inflammation promoting the removal of necrotic neural components and stimulating neo-vessel ingrowth, detrimental shifts in macrophage phenotype exacerbate nerve degeneration. Herein, we find that peripheral nerve injuries (PNIs) result in abundant secreted frizzled-related protein 1 (sFRP1) expression, particularly by Schwann cells (SCs). Heat shock protein 90 (HSP90) in macrophages recognizes sFRP1 and triggers a dysregulated secretion of inflammatory mediators. Single-cell atlas of human injured peripheral nerves reveals the appearance of sFRP1-expressing SCs with mesenchymal traits and macrophages with a proinflammatory genetic profile. Deletion of either SC-specific sFRP1 or macrophage-specific HSP90 alleviates neuroinflammation and prevents the progression of nerve degeneration. Together, our findings implicate the response of macrophages to SC-derived sFRP1 in exacerbating nerve damage following PNIs.

Clickable immune-microenvironment modulated hydrogels for spinal cord injury repair

Spinal cord injury (SCI) is a devastating condition without effective therapy currently available. The inflammatory cascade following SCI leads to neuronal apoptosis and glial cell activation. The utilization of local injectable hydrogels with immunotherapy drugs directly into injured nerve tissues represents a promising therapeutic strategy. Herein, injectable hydrogels grafted with clickable methylprednisolone (MP) and cellular adhesion peptide were developed using free radical polymerization for promoting nerve regeneration following SCI. MP conjugated hydrogels could modulate the immunoinflammatory microenvironment of SCI and sustain neuron survival. The multi-stiffness hydrogels were fabricated by adjusting concentration ratios to evaluate appropriate mechanical stimuli. In a model of dorsal root ganglion, MP grafted hydrogels with mechanical signals similar to those of adult rat spinal cords demonstrated superior efficacy in promoting dorsal root ganglion growth. MP grafted hydrogels could regulate the immune-inflammatory microenvironment, promote recovery of both motor function and sensory functions. The positive findings suggested that the interplay between immunomodulation and mechanical signals plays a crucial role in promoting nerve regeneration, indicating significant potential for hydrogels as a therapeutic approach for repairing SCI.

Spared ulnar nerve injury results in increased layer III–VI excitability in the pig somatosensory cortex

This study describes cortical recordings in a large animal nerve injury model. We investigated differences in primary somatosensory cortex (S1) hyperexcitability when stimulating injured and uninjured nerves and how different cortical layers contribute to S1 hyperexcitability after spared ulnar nerve injury. We used a multielectrode array to record single-neuron activity in the S1 of ten female Danish landrace pigs. Electrical stimulation of the injured and uninjured nerve evoked brain activity up to 3 h after injury. The peak amplitude and latency of early and late peristimulus time histogram responses were extracted for statistical analysis. Histological investigations determined the layer of the cortex in which each electrode contact was placed. Nerve injury increased the early peak amplitude compared with that of the control group. This difference was significant immediately after nerve injury when the uninjured nerve was stimulated, while it was delayed for the injured nerve. The amplitude of the early peak was increased in layers III–VI after nerve injury compared with the control. In layer III, S1 excitability was also increased compared with preinjury for the early peak. Furthermore, the late peak was significantly larger in layer III than in the other layers in the intervention and control group before and after injury. Thus, the most prominent increase in excitability occurred in layer III, which is responsible for the gain modulation of cortical output through layer V. Therefore, layer III neurons seem to have an important role in altered brain excitability after nerve injury.

Diagnostic Capability of Ultrasonography in Evaluating Peripheral Nerve Injuries of the Brachial Plexus.

The purpose of this study is to determine the diagnostic capability of ultrasonography (US) in patients with suspected brachial plexus injury (BPI) to the terminal nerves by comparing physical examination (PE) findings with US, electromyography (EMG), and magnetic resonance imaging (MRI) reports. All patients at a single institution who underwent US for peripheral nerve injury of the brachial plexus and terminal nerves resulting in sensory-motor deficits from October 1, 2017 to October 31, 2023 were identified. A retrospective chart review was performed. Each PE, US, EMG, and MRI reports were given an overall rating: "normal" or "abnormal." Terminal nerves (musculocutaneous, axillary, radial, ulnar, medial) were individually assessed as "normal" or "abnormal." The interobserver agreement between reports was calculated using Cohen kappa. Specificity and sensitivity analyses were performed to determine diagnostic accuracy and were reported with 95% confidence intervals (CI). A total of 120 patients were included. Most injuries were traumatic in nature (78.8%) and were low-energy (53.8%). When each imaging modality was compared with the PE findings, EMG had the highest interobserver agreement (Cohen kappa = 0.18), followed by US (Cohen kappa = 0.10), and last MRI (Cohen kappa = 0.07). The US had the highest sensitivity (0.92, CI = 0.85, 0.96) among the 3 imaging modalities (Table 2). On US, the ulnar nerve was most commonly abnormal (n = 84, 70.0%). Ultrasonography serves as a useful adjunct in the workup of patients with suspected peripheral BPI and is reliable in localizing the pathology of injured terminal nerves in the brachial plexus.

Ultrasonographic Evaluation of Morphological Changes in Peripheral Nerves after Traumatic Injury and Nerve Repair - A Prospective Study.

Purpose Ultrasound (US) has gained in importance for the visualization of morphological changes of injured nerves. After surgical repair, changes in neural structures are seen over time. The correlation of morphologic changes in US with the corresponding nerve function is uncertain. The aim of this study is to determine a correlation of post-traumatic morphological nerve changes with US and with nerve function after surgery. Materials and Methods This dual-center, prospective cohort study was conducted between 2017 and 2022 and included 20 mixed sensory motor nerve lesions. Patients were followed up clinically (sensitivity, pain, and motor function) with US and electroneuromyography. We determined the US changes of the nerves including the interaction of the tissue after nerve repair and any correlation with nerve function. With US nerve cross-sectional area (CSA), the number of traversing fascicles, hypo-echogenicity, and presence of perineural scar were analyzed. Results 20 lesions (12 median and 8 ulnar nerves) of 18 patients with intraoperatively confirmed nerve injury of at least 50% in the forearm were included. The average CSA was over 20 mm 2 throughout the follow-up period, corresponding to a neuroma in continuity compared to the opposite side (10.75 mm 2 ). Sensibility and motor function at 12 months were 6xS3/4 and 10xM3-5. There was a statistically significant correlation between continuous fascicles on US at 6 months and sensitivity at 12 months. Conclusion This study supports the presence of post-traumatic morphological changes in nerve fibers with US after traumatic injury. Morphological changes in nerve structure after trauma can be detected with US indicating a correlation between continuity of nerve fascicles and development of sensitivity and motor function.

Electromagnetic-responsive targeted delivery scaffold technology has better potential to repair injured peripheral nerves: a narrative review

Peripheral nerve injury with long size defects has been an urgent clinical challenge. With the development of bioengineering, nanotechnology and additive manufacturing technologies, biologic delivery systems have gradually shown great potential for the treatment of peripheral nerve injury. The main problem of general biologic delivery systems is that the loading capacity of biologics is positively correlated with the release rate, and it is more difficult to achieve long-term stable release of high biologics-loaded scaffolds; thus, it is not possible to carry out full-cycle targeted therapy for peripheral nerve injury sites. To solve these problems, the mechanisms of common neurotrophic factors, bioelectrical signals and biomagnetic signals for repairing peripheral nerve injury are discussed in this paper. Moreover, this review summarizes the mechanism of electroactive and magnetoresponsive materials that have significant ability to repair peripheral nerve injury to promote nerve regeneration and provides an overview of the biologic delivery mechanism for repairing peripheral nerve injury in different structural dimensions. It was finally concluded that electromagnetic responsive targeted delivery scaffolds (four-dimensional scaffolds) have good peripheral nerve repair ability, which provides guidance for the clinical application of targeted therapy for peripheral nerve injury.

Electrical Stimulation: Enhancing Axonal Growth following Peripheral Nerve Injury.

Electrical stimulation has been integrated in recent decades into rehabilitation protocols following neuromuscular injuries. Existing literature supports the utilisation of prolonged or continuous stimulation generated by implantable or transcutaneous devices for chronic pain subsidence and muscle trophism maintenance, which improve outcomes following microsurgical interventions. Newer uses include brief electrical stimulation for peripheral nerve injury. Brief electrical stimulation has shown promise in expediting regeneration of both torn and crushed nerve axons in the murine model and has been incorporated into a limited number of clinical studies. Augmentation of the natural response of an injured peripheral nerve by electrical stimulation has the potential to accelerate regeneration, presumably leading to improved function and clinical outcomes. We review the existing literature on intraoperative utilisation of electrical stimulation to enhance regeneration, such as neural mechanisms of action and their microscopic effect in animal models, as well as results from initial human studies. Level of Evidence: Level V (Therapeutic).

TFEB/3 Govern Repair Schwann Cell Generation and Function Following Peripheral Nerve Injury.

TFEB and TFE3 (TFEB/3), key regulators of lysosomal biogenesis and autophagy, play diverse roles depending on cell type. This study highlights a hitherto unrecognized role of TFEB/3 crucial for peripheral nerve repair. Specifically, they promote the generation of progenitor-like repair Schwann cells after axonal injury. In Schwann cell-specific TFEB/3 double knock-out mice of either sex, the TFEB/3 loss disrupts the transcriptomic reprogramming that is essential for the formation of repair Schwann cells. Consequently, mutant mice fail to populate the injured nerve with repair Schwann cells and exhibit defects in axon regrowth, target reinnervation, and functional recovery. TFEB/3 deficiency inhibits the expression of injury-responsive repair Schwann cell genes, despite the continued expression of c-jun, a previously identified regulator of repair Schwann cell function. TFEB/3 binding motifs are enriched in the enhancer regions of injury-responsive genes, suggesting their role in repair gene activation. Autophagy-dependent myelin breakdown is not impaired despite TFEB/3 deficiency. These findings underscore a unique role of TFEB/3 in adult Schwann cells that is required for proper peripheral nerve regeneration.

Enhancement of Heme-Oxygenase 1 in the Injured Peripheral Nerve Following Sulforaphane Administration Fosters Regeneration via Proliferation and Maintenance of Repair Schwann Cells.

Nuclear erythroid 2-related factor 2 (Nrf2) and its downstream effector heme oxygenase 1 (HO-1) are commonly activated in response to cellular stresses. The elevated expression of HO-1 has been associated with markedly accelerated peripheral nerve regeneration. This study aimed to evaluate the impact of a naturally occurring dietary Nrf2/HO-1 activator-sulforaphane (SFN)-on regeneration in a murine sciatic nerve crush model. The beneficial safety profile of SFN has been thoroughly investigated and confirmed several times. Here, SFN was administered daily, starting immediately after C57BL/6 mice were subjected to sciatic nerve crush injury. Injured sciatic nerves were excised at various time points post injury for molecular, immunohistochemical and morphometric analyses. Moreover, functional assessment was performed by grip strength analysis and electrophysiology. Following SFN treatment, the early response to injury includes a modulation of autophagic pathways and marked upregulation of Nrf2/HO-1 expression. This enhancement of HO-1 expression was maintained throughout the regeneration phase and accompanied by a significant increase in repair Schwann cells. In these cells, elevated proliferation rates were observed. Significant improvements in grip strength test performance, nerve conduction velocity and remyelination were also noted following SFN treatment. Collectively, SFN modulates cytoprotective and autophagic pathways in the injured nerve, increasing the number of repair Schwann cells and contributing to effective nerve regeneration. Given the availability of SFN as a nutritional supplement, this compound might constitute a novel regenerative approach with broad patient accessibility and further studies on this topic are warranted.

Effect of Tourniquet-Related Nerve Ischemia on Response to Handheld Nerve Stimulation in Ulnar Nerve Transposition.

Tourniquet-related nerve ischemia has been well studied in several reconstructive procedures, but the time-course of impaired response to intraoperative stimulation is unclear. The present study evaluated ischemic effects on conduction during ulnar nerve transposition and examined the relationship between intra- and pre- operative diagnostics. We hypothesized that intraoperative ischemia would have minimal impact on conduction. Thirty patients scheduled for anterior transposition were enrolled after preoperative examination, electrodiagnostic testing, and ultrasound. Demographic and symptom severity data were recorded. A handheld biphasic nerve stimulator was used intraoperatively to assess minimum amplitude and pulse duration needed for muscle response. Measurements were taken at 15-minute intervals after placement. Changes in threshold amplitude and pulse duration were calculated between each 15-minute interval; no significant difference was found in the change of either value (p = 0.70 and 0.178). A weak negative correlation existed between preoperative CMAP amplitudes and average intraoperative pulse duration, which increased to a moderate correlation when compared to 45-minute pulse duration (r=-0.62, p<0.01). Preoperative ulnar nerve cross-sectional area (CSA) demonstrated no significant correlation with average pulse duration but a moderate correlation with pulse duration at 45 minutes (r=0.63, p=0.01). Tourniquet use did not prevent effective intraoperative stimulation of the ulnar nerve for at least 45 minutes. The window for meaningful stimulation with tourniquet usage appears to be greater than previously thought. Preoperative nerve CMAP amplitude and CSA does appear to influence pulse duration required after 45 minutes of ischemia, suggesting that injured nerves are more susceptible to ischemia. 1.

Upper Extremity Ballistic Nerve Injury

» Gunshot injuries to the upper extremity (UE) have high likelihood for causing peripheral nerve injury secondary to the high density of vital structures. Roughly one-fourth of patients sustaining a gunshot wound (GSW) to the UE incur a nerve injury. Of these nerve injuries, just over half are neurapraxic. In cases of surgical exploration of UE nerve injuries, nearly one-third demonstrate a transected or discontinuous nerve.» Existing literature regarding surgical management of nerve injuries secondary to GSWs comes from both military and civilian injuries. Outcomes are inconsistently reported, and indications are heterogeneous; however, reasonable results can be obtained with nerve reconstruction.» Our proposed management algorithm hinges on 4 treatment questions: if there is a nerve deficit present on examination, if there is a concomitant injury in the extremity (i.e., fracture or vascular insult), whether the injured nerve would be in the operative field of the concomitant injury, and whether there was an identified nerve lesion encountered at the time of surgery by another surgeon?» Early exploration rather than continued expectant management may offer improved recovery from GSW nerve injuries in particular situations. When an UE nerve deficit is present, establishing follow-up after the initial GSW encounter and early referral to a peripheral nerve surgeon are pivotal.

Neuritin accelerates Schwann cell dedifferentiation via PI3K/Akt/mTOR signalling pathway during Wallerian degeneration.

Neuritin, also known as candidate plasticity gene 15 (CPG15), was first identified as one of the activity-dependent gene products in the brain. Previous studies have been reported that Neuritin induces neuritogenesis, neurite arborization, neurite outgrowth and synapse formation, which are involved in the development and functions of the central nervous system. However, the role of Neuritin in peripheral nerve injury is still unknown. Given the importance and necessity of Schwann cell dedifferentiation response to peripheral nerve injury, we aim to investigate the molecular mechanism of Neuritin steering Schwann cell dedifferentiation during Wallerian degeneration (WD) in injured peripheral nerve. Herein, using the explants of sciatic nerve, an exvivo model of nerve degeneration, we provided evidences indicating that Neuritin vividly accelerates Schwann cell dedifferentiation. Moreover, we found that Neuritin promotes Schwann cell demyelination as well as axonal degeneration, phagocytosis, secretion capacity. In summary, we first described Neuritin acts as a positive regulator for Schwann cell dedifferentiation and WD after peripheral nerve injury.

SCOPING: A Pilot Study Exploring the Role of A Series of Clinical Observational Parameters as Indicators of Nerve Regeneration.

Following the repair of a mixed peripheral nerve, functional recovery requires successful nerve regeneration across the repair site and, eventually, reinnervation of distal targets. Reliably determining a failing nerve repair so that revision may be performed before irreversible muscle atrophy remains a challenge in peripheral nerve surgery. This study aimed to ascertain whether any commonly used clinical examination tests during surveillance after nerve repair can detect a failing repair and prompt earlier salvage intervention. A prospective observational cohort study was performed to evaluate commonly used clinical determinants of neuron regeneration that may provide early surrogate recovery measures. Sequential cutaneous thermography was used to identify temperature differences between denervated and normal skin in the hand operated on, with the contralateral hand as a control. Six out of nine patients completed between 6 and 18 months of follow-up. Tinel sign progression was observed in all subjects. Tinel progression rate was associated with motor and sensory Medical Research Council grade. The delta temperature was calculated to document the size and direction of any temperature differentials in the hand detected by thermography, but we did not have sufficient data to calculate any correlations with motor and sensory Medical Research Council grade. Specifically, the progression of Tinel sign is associated with recovery measured by progression of the British Medical Research Council motor and sensory grades. The use of thermographic imaging demonstrates that there is a difference in temperature between an injured and noninjured nerve. Future studies could investigate to what extent thermographic imaging predicts final nerve repair outcomes.

Trigeminal nerve injuries following dental procedures: A retrospective analysis of malpractice claims from 2016 to 2023 in South Korea

BackgroundDental malpractice claims, which pertain to legal actions against dentists accused of clinical negligence that caused harm to patients, have increased in the past ten years in South Korea. The claims are caused by complications, particularly trigeminal nerve injuries, resulting from various dental procedures. Medicolegal issues related to trigeminal nerve injury have not been previously described in South Korea. Therefore, in this study, we aimed to identify the general, dental, and judicial characteristics of closed dental malpractice claims. MethodsThis study was designed as a descriptive study. We collected the data of 51 closed claims related to trigeminal nerve injury resulting from dental procedures such as dental implant emplacement, tooth extraction, and local anesthesia. The claims were decided by courts in South Korea between 2016 and 2023. The general, dental, and judicial characteristics of the claims were analyzed retrospectively. ResultsThe average claim resolution period was 4.2 (range: 1.47–8.39) years post-adverse events that occurred more frequently in dental clinics (68.6 %) than in dental (25.5 %) or general hospitals (5.9 %). Inferior alveolar (66.7 %) and lingual (17.6 %) nerves were injured following dental procedures. The duty to inform was breached in 68.6 % of claims. The dental procedure performed (P < 0.001) and the injured nerve (P < 0.001) were associated with the violation of the duty to care. ConclusionTo improve the quality of dental care services, the analysis of the adverse events using various resources including judgments should be strongly addressed.