Conventional peripheral neurorrhaphy techniques often yield suboptimal functional outcomes. The addition of polyethylene glycol (PEG), a hydrophilic polymer, has emerged as a promising adjunct to enhance axonal regeneration and expedite recovery following nerve transection. This manuscript provides a comprehensive overview of the biochemical properties of PEG with its unique features used in peripheral nerve injuries, and the technical considerations underlying its application in acute peripheral nerve repair. We review preclinical and clinical literature evaluating PEG-mediated axonal fusion, including meta-analyses of animal studies and recent human trials. Emphasis is placed on PEG's mechanism of action, as well as the role of complementary agents such as methylene blue. Additionally, we describe our institution's standardized surgical protocol for PEG-assisted end-to-end neurorrhaphy, supported by intraoperative technical rationale. Data from rodent models and human patients consistently demonstrate accelerated sensory and motor recovery when PEG is integrated into neurorrhaphy protocols. PEG's nonspecific dehydration of axonal membranes facilitates immediate axonal fusion, restoring neural continuity and reducing the latency of regenerative processes. Clinical outcomes are particularly favorable in clean transections repaired within 72 hours, with no significant PEG-related adverse events reported to date. PEG-mediated fusion represents a potential enhancement to standard microsurgical nerve repair. While further investigation is needed to optimize application parameters, address axonal specificity, and define long-term efficacy, current evidence supports PEG as a safe, effective, and accessible technique to improve outcomes in peripheral nerve repair.

The parasympathetic nervous system (PNS), a division of the autonomic nervous system, maintains physiological homeostasis within the body. The PNS seems to influence the processing of nociceptive information. A growing body of research indicates that the PNS actively contributes to various pain conditions associated with inflammation of tissues and/or neural damage. Therefore, the aim of this review is to integrate current findings regarding the peripheral parasympathetic pathways implicated in pain, encompassing direct cholinergic actions and indirect effects on the sensory nervous system. Enhanced insight into PNS-sensory interactions in pain could provide a basis for identifying new strategies for the prevention and management of pain conditions.

A significant, yet often overlooked, complication of subarachnoid hemorrhage (SAH) is the development of acidosis. Denervation atrophy is a recognized cause of neural ganglion damage following primary motor neuron damage, but the effect of tissue pH changes has not been thoroughly investigated. This study investigates whether acidosis causes Auerbach ganglia damage following SAH. Twenty-four hybrid rabbits were selected, and five (GI; n = 5) were used for the analysis of the Auerbach ganglia. Six animals (GII; n = 6) were allocated to the SHAM group, receiving 1 cc of saline. The remaining 13 animals (GIII; n = 13) were allocated to the study group, receiving 1 cc of autologous arterial blood injected into the cisterna magna to induce subarachnoid hemorrhage under general anesthesia. Blood pH values were recorded before the experiment, on the seventh day, and immediately before sacrifice. Animals were sacrificed after 1 week, and the degenerated neuron density of the Auerbach ganglia in 1 cm segments of the ascending colon was estimated. The pH values and degenerated Auerbach ganglia neuron densities (n/mm3) were compared using the Mann-Whitney U test. The presurgical blood pH values of all animals were 7.431 ± 0.032. On the seventh day, pH values were 7.403 ± 0.052 in GI; 7.395 ± 0.024 in GII; and 7.264 ± 0.045 in GIII. At the end of the experiment, pH values were 7.431 ± 0.037 in GI; 7.395 ± 0.062 in GII; and 7.330 ± 0.035 in GIII. Degenerated neuron densities of Auerbach ganglia neurons were 13 ± 4 in GI, 34 ± 6 in the SHAM group, and 87 ± 15 in GIII. The p values were: p < 0.005 for GII/GI; p < 0.0001 for GII/GIII; and p < 0.00005 for GI/GIII. Acidosis is a potential causative factor of Auerbach ganglia degeneration following SAH, a phenomenon not previously described.

An early rapamycin-releasing nerve wrap with dual function for nerve regeneration and adhesion prevention.

Cavidine alleviates paclitaxel-induced peripheral neuropathy by promoting mitochondrial autophagy through inhibiting PKM2-mediated histone lactylation.

Axonal spheroids are regulated by Schwann cells after peripheral nerve injury

Mesenchymal stem cell-laden double-network hydrogel nerve guidance conduits for peripheral nerve injury repair.

Interleukin 13 alleviates traumatic brain injury by promoting pericyte autophagy.

Application of Traditional Chinese Medicine in the different pathological stages of ischemic stroke: Target immune cells.

Type 3 resistant starch from Canna edulis improves Parkinson's symptoms, including behavioral function and nerve damage, in Parkinson's model rats by regulating the gut-brain axis.

This study aims to examine the effect of the chitosan/polyethylene oxide (Cs/PEO) scaffold on sciatic nerve regeneration and neural tissue angiogenesis in adult male rats. Thirty two rats were divided into normal, control, sham and Cs/PEO groups. In the control, sham and Cs/PEO groups, the sciatic nerve was severed in the middle region of the thigh, and epineuria was sutured. After 8 weeks, the functional recoveries, the nerve conduction velocity (NCV), the nerve fiber number, the largest nerve fiber area (LNFA), the largest axon area (LAA) and the number of blood vessels were evaluated. Nerve fiber numbers showed a statistically significant increase in the Cs/PEO, control and sham relative to the normal group. The mean size of the LAA and blood vessels indicated a significant increase in the Cs/PEO group in comparison with the others and the normal group, respectively. The study demonstrated that nerve regeneration with epineural sutures and Cs/PEO could prevent fatal neuron changes and promote angiogenesis following sciatic nerve injury particularly in the first 2 weeks, which rescue some neurons in this initial vital time of injury. However, the Cs/PEO scaffold alone may not be sufficiently effective in sciatic nerve regeneration over a long time period.

The injury to neurons and connection structures in the nervous system is a key factor leading to neurodegenerative diseases. Self-repair function refers to the innate capacity of the neuron-astrocyte network to partially restore or maintain its function following injury, without external intervention. When the brain's nervous system is injured, how self-repair mechanisms work under various injury conditions and how to improve self-repair function remain unresolved. Through computational simulations of three distinct neurological injury scenarios, we investigated the self-repair function of spiking neuron-astrocyte networks in working memory tasks. Despite varying degrees of disruption of the network, all experiments (Self-Repair activated by synaptic connection injury, astrocytes injury, and internal noise interference) reveal that astrocytes can promote self-repair of the network during working memory tasks. Experiments on synaptic connection injury demonstrated that the network can maintain effective repair functionality under high injury conditions, which is associated with elevated calcium ion concentrations induced by increased glutamate release from presynaptic neurons. The modulation of astrocyte contributes to self-repair, and self-repair function decreases with increasing astrocyte injury. In addition, compared to the health network, internal noise interference has a small enhancement in the self-repair function of the network. Our findings elucidate the critical role of astrocyte-mediated signaling in maintaining network under different synaptic injury. This provides novel mechanistic insights into the threshold dynamics governing neuron network stability and early pathological transition in response to diverse neural injuries.

A near-infrared ratiometric optical sensor for real-time monitoring hydroxyl radical levels in ferroptosis-mediated Parkinson's disease.

Toxicological effects of diquat on the central nervous system and associated treatment challenges.

Long-gap peripheral nerve injury (PNI) presents a significant challenge since the growth cone at the proximal end fails to detect and respond to neurotrophic signals from the distal ends, even when bridging the long-gap with nerve guide conduits (NGCs), impeding the motivated growth of new axons. In this study, a bioinspired force-inducible multichannel nerve guide conduit (FI-MNGC) is developed, constructed from silk fibrin-based hydrogel. By mimicking the gradient capillary architectures in vascular plants, the FI-MNGC utilizes a multichannel design with gradient apertures that can self-generate enhanced capillary forces, which not only promote directed axon growth but also guide the directed delivery of Schwann cells (SCs) toward the distal ends of the injured nerve, without the need for any external stimuli. Implemented in a rat model with a 16mm and a rabbit model with a 30mm long-gap sciatic nerve defect, the FI-MNGC significantly accelerates the recovery process, paralleling the efficacy of autografts in nerve regeneration, functional recovery, and repair speed. This innovative approach offers a promising alternative to autografts, enhancing the potential for clinical implementation in long-gap PNI therapies.

To evaluate structural and microvascular changes in the macular retina and choroid of patients with chronic primary angle-closure glaucoma (CPACG) following trabeculectomy, using ultra-widefield swept-source optical coherence tomography angiography (UWF SS-OCTA). This prospective observational study included 40 eyes from CPACG patients undergoing trabeculectomy and 42 eyes from age- and sex-matched healthy controls. UWF SS-OCTA was used to quantify macular parameters including superficial vascular density (SVD) values, ganglion cell complex (GCC) thickness values, choroidal thickness (CT) values, choriocapillaris flow density (CCD) values, and choroidal vascularity index (CVI) values at baseline, 1 week, and 1 month postoperatively. At baseline, the CPACG group showed significantly reduced SVD, GCC thickness, and CVI values, along with diffusely increased CT values compared to healthy controls. After trabeculectomy, IOP was significantly reduced at both 1 week and 1 month. SVD and CVI values significantly improved by 1 month postoperatively, suggesting early microvascular recovery. CT values peaked at 1 week and declined by 1 month, while CCD values showed no significant changes. GCC thickness values remained stable postoperatively, indicating irreversible neuroaxonal damage. CPACG patients exhibit concurrent retinal-choroidal structural impairment and microcirculatory dysfunction. Trabeculectomy leads to partial reversal of microvascular deficits, particularly in SVD and CVI values. However, the irreversibility of neural damage highlights the necessity for early detection and timely intervention in CPACG management.

Dynamic mechanical cues are crucial for glial neuromodulation and energy metabolism in neural regeneration, yet the mechanisms underlying mechanotransduction and intracellular organelle responses in glia after neurotrauma remain vague. In this study, we develop mechano-bioactive piezoelectric hydrogel bioelectronics (BaTiO3-embedded collagen-1 hydrogel) and investigate mechanotransduction in astrocytes and Schwann cells. Ultrasound-driven piezoelectric hydrogel bioelectronics exerts electrical signals from mechanical stimulation and upregulates PIEZO1 channel in astrocytes and PIEZO2 channel in Schwann cells. This mechanoelectrical conversion increases calcium influx to activate ATP synthase subunit and promote MFN/OPA1 mediated mitochondrial fusion. Consequently, it enhances ATP synthesis by forming an efficient energy network as a central bioenergetic hub to promote glia mediated neural repair. Furthermore, this mechano-bioactive piezoelectric hydrogel bioelectronics exhibits therapeutic efficacy for treating central and peripheral nervous injuries in multiple animal models (mice, rats, Beagle dogs, and Rhesus monkeys), demonstrating its wide adaptivity and significant translational potential. The findings elucidate a multilevel mechanobiological energy transduction (mechanical-electrical-bioenergetic conversion) design in neural repair as a promising clinical treatment mode.

Following open thoracoabdominal surgery, patients are at risk of chronic pain due to unintentional peripheral nerve injury (PNI), such as nerve transection, compression, or stretching of peripheral nerves. While laparoscopic surgery is minimally invasive, the incidence of subsequent PNI from laparoscopic surgery remains unknown. PubMed, Embase, Web of Science, and Scopus databases were searched for peer-reviewed literature discussing nerve injuries following open or laparoscopic thoracoabdominal surgeries. From 1,580 unique citations, 28 articles (n = 871 patients) qualified for inclusion. There were 555 (63.7%) males and 316 (36.3%) females. The mean age was 54.5 ± 9.6, ranging from 18 to 92. Following 451 open thoracoabdominal surgeries, there were 214 nerve injuries (47.5%). Following 420 laparoscopic thoracoabdominal surgeries, there were 22 nerve injuries (5.2%). Laparoscopic surgery had statistically significantly lower PNI (p < 0.0001) than open procedures. These procedures caused 236 reported cases of PNI, which included neuromas (50.4%), nerve enlargement (37.3%), nerve transection (8.5%), nerve entrapment (2.5%), perineural inflammation (2.2%), and nerve crush injury (0.4%). Of patients with PNI, surgery was performed on 170 (72.0%) patients and non-surgical treatments were given in 64 (27.1%) patients. The surgical interventions for PNI included neurectomy (78.8%), neuroma excision (19.4%), and scar excision (1.8%). A laparoscopic approach, versus a surgical open approach to treat thoracoabdominal surgical problems, has decreased the risk of inadvertent nerve injuries. The wide variation in the description of the types of injuries is indicative of the generally poorly understood nature of peripheral nerve injuries, indicating an opportunity for greater emphasis on the diagnosis and treatment of this problem.

ABSTRACTThe neural mechanisms of handedness remain poorly understood, particularly for lateralized movements such as precision drawing. Using functional magnetic resonance imaging (fMRI), we examined how healthy adults and individuals with peripheral nerve injury (PNI) in their dominant hand performed a visually guided drawing task with each hand. We hypothesized that the left superior parietal lobule (SPL) supports drawing with either hand, and that individuals with PNI would recruit the same mechanisms as healthy adults.Methods33 Right-handed adults (23 healthy adults, 10 patients) underwent fMRI while performing a precision drawing task, alternating between the right hand (RH) and left hand (LH). LH>RH effects were examined across 20 regions of interest (12 a priori, 8 post hoc) using two approaches: (1) BOLD magnitude, and (2) functional connectivity (FC) modulation, assessed via generalized psychophysiological interaction.ResultsAll effects describe LH drawing > RH drawing. Right primary motor cortex (M1) had lower magnitude and greater FC with two networks, both of which exhibited equal-or-greater magnitude: a left hemisphere M1-dorsal premotor circuit, and an intrahemispheric parieto-temporal circuit. Right M1 (also had reduced interhemispheric FC with inferior parietal lobule, which exhibited lower magnitude. Patient group had no effect on magnitude or FC.ConclusionsThree neural mechanisms differentiate LH from RH drawing in right handed adults. First, a left hemisphere system for bimanual control, which engages intrahemispherically (directly) during RH drawing but interhemispherically (indirectly) during LH drawing. Second, LH drawing increases engagement of a contralateral system that may reflect increased task demands. Third, RH drawing increases engagement of an interhemispheric circuit for tool use. The first and third systems may explain performance asymmetries associated with handedness. Patients with PNI use the same mechanisms as healthy adults, highlighting these mechanisms’ potential as a neuromodulatory target to enhance LH performance after RH impairment.

Perioperative peripheral nerve injury (PNI) and impaired repair constitute a common pathological mechanism triggering acute and chronic postoperative pain. The current key challenge lies in the difficulty of achieving synergistic intervention for both excessive inflammation in the acute phase and the lack of neural structure during the repair phase. Accordingly, this study constructs an IL-10-engineered injectable short fiber (IL10-mPDA@SF) system based on immune-structure synergistic regulation to promote peripheral nerve repair and suppress acute and chronic postoperative pain. On one hand, IL10-mPDA@SF achieves immune regulation by locally and continuously releasing IL-10, which effectively induces macrophage polarization toward the M2 phenotype by activating macrophage surface receptors. This remodels the anti-inflammatory microenvironment and blocks neuronal hyperexcitability. On the other hand, its extracellular matrix (ECM)-like short fiber structure provides physical guidance for the directional migration of Schwann cells and the orderly regeneration of nerve axons, thereby inhibiting the traumatic neuroma formation and achieving guided neural structural regeneration. In vitroexperiments demonstrate the effectiveness of this dual-modal synergistic mechanism. In a mouse plantar incision model, local injection of IL10-mPDA@SF significantly reduces the acute mechanical hypersensitivity threshold by over 50%, promotes the repair of nerve function and wounds, and suppresses traumatic neuroma occurrence.