A 60-year-old male patient came to the outpatient department with the complaint of gradual, painless, progressive diminishing of vision in right eye for two months. His medical history included diabetes mellitus type II, hypertension, and hypercholesterolaemia for eight years. Best corrected visual acuity on snellen's chart for distance was 6/9 in right eye and 6/6 in left eye and for near was N6 in both eyes. Colour vision was intact bilaterally and there was no relative afferent pupillary defect. Anterior segments findings were within normal limits. Fundus examination revealed superior disc pallor and inferiorly showed hyperaemia with dilated vessels. Humphrey visual field testing showed incomplete inferonasal field loss in the right eye which correlated with the disc findings of superior disc pallor. OCT-A showed various pattern changes in the retinal peripapillary capillaries like capillary dropout areas in the temporal region, increase in the vessel density in non-ischaemic areas depicting luxury perfusion, dilatation, and tortuosity of small and large vessels with loss of their radial pattern. Here we describe a unique case where optical coherence tomography angiography (OCT-A) was a helpful investigation in diagnosing luxury perfusion in a patient of Non Arteritic anterior ischaemic optic neuropathy (NAION).

Radial sorting of axons is a critical process in nerve development, ensuring proper segregation of axons to form myelinated and unmyelinated Schwann cell-axon units. This process is tightly regulated by signals that mediate communication between Schwann cells and the extracellular matrix, with laminin-211 being one of the key players. However, the molecular signals involved in directing Schwann cell-axon interactions are less understood, highlighting the need to identify additional molecules that mediate axon recognition and segregation. Gaining a deeper understanding of these mechanisms may shed light on the pathogenesis of genetic neuropathies. In this study, we utilized a mouse model of either sex with defects in axonal sorting, resulting from the conditional inactivation of the COP9 signalosome component Csn5 (Jab1) in Schwann cells. Transcriptome analysis was performed to identify adhesion molecules dysregulated during nerve development. Notably, we discovered that the repulsive molecule Slit2 was significantly overexpressed in Jab1-KO nerves and was particularly abundant in axon bundles with improper sorting. We demonstrated that while Slit2 is highly expressed in embryonic nerves, its expression must be precisely regulated in mature Schwann cells. Gain- and loss-of-function mutants for Slit2 further confirmed the role of Slit2 in nerve development. Transgenic mice overexpressing Slit2 displayed defects in radial sorting and hypomyelination, while Slit2 loss led to hypermyelination and misalignment of unmyelinated axons in Remak bundles. Additionally, Slit2 dysregulation interfered with nerve regeneration following cut injury. Our findings suggest that Slit2 plays a significant role in multiple stages of nerve development and some aspects of nerve regeneration.Significance Statement Nerve development and regeneration following injury depend on intricate interactions between Schwann cells, axons, and their surrounding environment. Using both gain- and loss-of-function models, we identify a critical role for the inhibitory molecule Slit2 in regulating radial axon sorting, axonal alignment, myelination, and axon regeneration.

It is important to recognize neurological symptoms postemergency or elective surgery of the upper limb, as it could herald injury to the peripheral nerves. Prompt diagnosis, workup, and management of these conditions may affect eventual clinical outcomes. We present a series of cases in different orthopaedic-related scenarios to discuss the variety of causes and treatment options available for this group of patients. This study reflects level of evidence V.

The sciatic nerve is the largest nerve in the human body and is frequently affected by lesions, causing pain and even loss of sensitivity. The sciatic nerve injury model provides a robust platform to study the degeneration-regeneration process. In this context, Schwann cells (SC) are central regulators of peripheral nervous system (PNS) development, homeostasis, and regeneration. During development, SC arise from neural crest-derived precursors and undergo tightly regulated lineage progression, culminating in myelinating and non-myelinating phenotypes. This process is orchestrated by coordinated transcriptional, signaling, and epigenetic mechanisms that control radial sorting, differentiation, and myelination. Following nerve injury, SC exhibit remarkable plasticity, reprogramming into a specialized repair phenotype that promotes axonal regeneration through debris clearance, trophic support, immune modulation, and the formation of Büngner bands. This work aims to summarize the known history of the plasticity and functions of SC during nerve development and regeneration. It also aims to highlight the most recent advances regarding the molecular networks underlying SC plasticity, as well as epigenetic regulators that enable dynamic transitions between cellular states. This work also describes the factors compromising nerve regeneration and functional recovery, and summarizes the emerging therapeutic strategies aimed to overcome these limitations by enhancing SC plasticity, modulating the injury microenvironment, and developing alternative cell sources, including stem cell-derived Schwann-like cells. A deeper understanding of SC heterogeneity, lineage dynamics, and regenerative mechanisms will be essential for advancing translational strategies. Collectively, this review underscores the pivotal role of SC in nerve regeneration and highlights innovative approaches to harness their therapeutic potential.

A 37-year-old female patient was misdiagnosed with radial neuroma due to thumb weakness. After surgery, the weakness of her upper limbs worsened over 4 months. The most obvious symptoms upon admission were drooping wrists and inability to straighten the five fingers. Electromyography showed left radial nerve injury. She was preliminarily diagnosed with radial neuritis. The patient was treated with ultrasound-assisted electroacupuncture for 6 months, and the muscle strength of the upper limbs increased significantly. This case suggests that ultrasound-guided localization and electroacupuncture therapy are the key methods in treating radial neuritis.