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Introduction: Double-crush syndrome (DCS) represents a condition that involves peripheral nerve compression in combination with spinal nerve root impingement. The purpose of this study was to compare electrodiagnostic study (EDS) results in patients undergoing carpal tunnel release (CTR) for carpal tunnel syndrome with those undergoing both CTR and anterior cervical diskectomy and fusion for DCS., Methods: Patients receiving an isolated CTR were compared with those undergoing CTR and anterior cervical diskectomy and fusion within two years of CTR. The latter group was defined as our DCS cohort. Electrodiagnostic study results were collected which included sensory and motor nerve conduction data as well as electromyogram (EMG) findings. All electrodiagnostic studies were done before CTR in both sets of patients., Results: Fifty-four patients with DCS and 137 CTR-only patients were included. Patients with DCS were found to have decreased sensory onset latency (3.51 vs 4.01; P = 0.015) and peak latency (4.25 vs 5.17; P = 0.004) compared with the CTR-only patients. Patients with DCS had slower wrist motor velocity (30.5 vs 47.7; P = 0.012), decreased elbow motor latency (9.62 vs 10.6; P = 0.015), and faster elbow motor velocity (56.0 vs 49.4; P = 0.031). EMG results showed that patients with DCS were more likely to have positive findings in the biceps (31.9% vs 1.96%; P < 0.001) and triceps (24.4% vs 2.97%; P < 0.001), but not abductor pollicis brevis (APB) (45.7% vs 37.9%; P = 0.459)., Conclusion: We identified changes on EDS between patients with and without DCS. In patients with DCS, sensory nerve studies showed shorter peak and onset latency than in CTR-only patients. Interestingly, DCS and CTR-only patients had different patterns of wrist and elbow motor nerve conduction. Providers observing positive EMG findings proximal to the APB should raise their suspicion for possible cervical radiculopathy and when present with carpal tunnel syndrome-like symptoms, should also consider DCS in their diagnostic differential., (Copyright © 2024 by the American Academy of Orthopaedic Surgeons.)

Glucose, the primary cellular energy source, is metabolized through glycolysis initiated by the rate-limiting enzyme hexokinase (HK). In energy-demanding tissues like the brain, HK1 is the dominant isoform, primarily localized on mitochondria, and is crucial for efficient glycolysis-oxidative phosphorylation coupling and optimal energy generation. This study unveils a unique mechanism regulating HK1 activity, glycolysis and the dynamics of mitochondrial coupling, mediated by the metabolic sensor enzyme O-GlcNAc transferase (OGT). OGT catalyses reversible O-GlcNAcylation, a post-translational modification influenced by glucose flux. Elevated OGT activity induces dynamic O-GlcNAcylation of the regulatory domain of HK1, subsequently promoting the assembly of the glycolytic metabolon on the outer mitochondrial membrane. This modification enhances the mitochondrial association with HK1, orchestrating glycolytic and mitochondrial ATP production. Mutation in HK1's O-GlcNAcylation site reduces ATP generation in multiple cell types, specifically affecting metabolic efficiency in neurons. This study reveals a previously unappreciated pathway that links neuronal metabolism and mitochondrial function through OGT and the formation of the glycolytic metabolon, providing potential strategies for tackling metabolic and neurological disorders., (© 2024. The Author(s), under exclusive licence to Springer Nature Limited.)