Objective: To investigate the effect of combined repetitive peripheral magnetic stimulation and transcranial magnetic stimulation on upper extremity function in subacute stroke patients. Design: Pilot study. Subjects: Subacute stroke patients. Methods: Included patients were randomized into 3 groups: a central-associated peripheral stimulation (CPS) group, a central-stimulation-only (CS) group, and a control (C) group. The CPS group underwent a new paired associative stimulation (combined repetitive peripheral magnetic stimulation and transcranial magnetic stimulation), the CS group underwent repetitive transcranial magnetic stimulation, and the C group underwent sham stimulation. All 3 groups received physiotherapy after the stimulation or sham stimulation. The treatment comprised 20 once-daily sessions. Primary outcome was the Fugl-Meyer Assessment Upper Extremity (FMA-UE) score, and secondary outcomes were the Barthel Index and Comprehensive Functional Assessment scores, and neurophysiological assessments were mainly short-interval intracortical inhibition. A 3-group (CPS, CS, C) × 2-time (before, after intervention) repeated measures analysis of variance was conducted to determine whether changes in scores were significantly different between the 3 groups. Results: A total of 45 patients were included in the analysis. Between-group comparisons on the FMA-UE demonstrated a significant improvement (group × time interaction, F2,42 = 4.86; p = 0.013; C vs CS, p = 0.020; C vs CPS, p = 0.016; CS vs CPS, p = 0.955). Correlation analysis did not find any substantial positive correlation between changes in FMA-UE and short-interval intracortical inhibition variables (C, r = –0.196, p = 0.483; CS, r = –0.169, p = 0.546; CPS, r = –0.424, p = 0.115). Conclusion: This study suggests that the real-stimulus (CS and CPS) groups had better outcomes than the control (C) group. In addition, the CPS group showed a better trend in clinical and neurophysiological assessments compared with the CS group.

Microglia, which are the resident macrophages and the first line of defense in the brain, can be activated within hours and migrate toward the injury sites after acute and chronic ischemic brain injury. However, a few studies have reported the interaction between microglia activation and necroptosis signaling following ischemic damage to the brain. In this study, chronic ischemic brain injury was induced by bilateral carotid artery stenosis (BCAS) and mice were sacrificed at 30 days after surgery. Ionized calcium-binding adaptor molecule 1 (IBA1) and glial fibrillary acidic protein (GFAP) immunostaining were performed to determine glial cell activation and inflammatory response. Tumor necrosis factor-α (TNF-α), interferon-γ (INF-γ), and interleukin-1β (IL-1β) proteins from the brains were examined to confirm inflammatory cytokines after BCAS. RIP1 and RIP3 proteins were detected to determine necroptosis signaling by Western blot. The data suggested that inflammatory responses, microglia activation, and necroptosis signaling are features of brain tissue pathology following BCAS-induced chronic ischemic brain injury.

Patients with recurrent glioblastoma often opt for hypofractionated stereotactic radiosurgery, which can cause various adverse reactions. The pharmacological interventions used to manage these adverse reactions are usually unsatisfactory. The present study reports the case of a patient with recurrent glioblastoma who underwent hyperbaric oxygen therapy followed by immediate hypofractionated stereotactic radiosurgery. Grip strength, isokinetic muscle testing and gait analysis were evaluated during the treatment period, spanning an interval of 7 days in March 2023. Assessments before and after treatment revealed improvements in all three parameters compared with pre‑treatment levels. In summary, combining hyperbaric oxygen therapy with hypofractionated stereotactic radiosurgery may enhance muscle strength in patients with recurrent glioblastoma. This treatment approach can lead to significant improvements in gait parameters, promoting better motor coordination. Furthermore, the combined therapy could offer a promising alternative for managing muscle weakness and mobility issues after glioblastoma recurrence.

JOURNAL/nrgr/04.03/01300535-202512000-00026/figure1/v/2026-04-22T170925Z/r/image-tiff Promoting synaptic plasticity and inducing functional reorganization of residual nerve fibers hold clinical significance for restoring motor function following spinal cord injury. Neuromagnetic stimulation targeting the nerve roots has been shown to improve motor function by enhancing nerve conduction in the injured spinal cord and restoring the synaptic ultrastructure of both the sensory and motor cortex. However, our understanding of the neurophysiological mechanisms by which nerve root magnetic stimulation facilitates motor function recovery in the spinal cord is limited, and its role in neuroplasticity remains unclear. In this study, we established a model of spinal cord injury in adult male Sprague–Dawley rats by applying moderate compression at the T10 vertebra. We then performed magnetic stimulation on the L5 nerve root for 3 weeks, beginning on day 3 post-injury. At day 22 post-injury, we observed that nerve root magnetic stimulation downregulated the level of interleukin-6 in the injured spinal cord tissue of rats. Additionally, this treatment reduced neuronal damage and glial scar formation, and increased the number of neurons in the injured spinal cord. Furthermore, nerve root magnetic stimulation decreased the levels of acetylcholine, norepinephrine, and dopamine, and increased the expression of synaptic plasticity-related mRNA and proteins PSD95, GAP43, and Synapsin II. Taken together, these results showed that nerve root magnetic stimulation alleviated neuronal damage in the injured spinal cord, regulated synaptic plasticity, and suppressed inflammatory responses. These findings provide laboratory evidence for the clinical application of nerve root magnetic stimulation in the treatment of spinal cord injury.