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High-voltage electrocution is mostly unintentional, and it is associated with significant morbidity and mortality due to severe tissue damages. The present report describes an atypical electrocution with multiple victims and a fatal outcome of a 48-year-old man due to unusual neck injuries caused by accidental electrical burns.

The lungs and the immune and nervous systems functionally interact to respond to respiratory environmental exposures and infections. The lungs are innervated by vagal sensory neurons of the jugular and nodose ganglia, fused together in smaller mammals as the jugular-nodose complex (JNC). Whereas the JNC shares properties with the other sensory ganglia, the trigeminal (TG) and dorsal root ganglia (DRG), these sensory structures express differential sets of genes that reflect their unique functionalities. Here, we used RNA sequencing (RNA-seq) in mice to identify the differential transcriptomes of the three sensory ganglia types. Using a fluorescent retrograde tracer and fluorescence-activated cell sorting, we isolated a defined population of airway-innervating JNC neurons and determined their differential transcriptional map after pulmonary exposure to lipopolysaccharide (LPS), a major mediator of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) after infection with gram-negative bacteria or inhalation of organic dust. JNC neurons activated an injury response program, leading to increased expression of gene products such as the G protein-coupled receptor Cckbr, inducing functional changes in neuronal sensitivity to peptides, and Gpr151, also rapidly induced upon neuropathic nerve injury in pain models. Unique JNC-specific transcripts, present at only minimal levels in TG, DRG, and other organs, were identified. These included TMC3, encoding for a putative mechanosensor, and urotensin 2B, a hypertensive peptide. These findings highlight the unique properties of the JNC and reveal that ALI/ARDS rapidly induces a nerve injury-related state, changing vagal excitability.

Occipital condylar fractures (OCFs) causing delayed onset lower cranial nerve paralysis (LCNPs) are rare. We present a 7-year-old Friesian horse with delayed onset dysphagia caused by vagus nerve (CNX) paralysis and suspicion of glossopharyngeal nerve (CNIX) paralysis developed several days after a minor head injury. Endoscopic examination revealed right laryngeal hemiplegia and intermittent dorsal displacement of the soft palate. An area of submucosal hemorrhage and bulging was appreciated over the dorsal aspect of the medial compartment of the right guttural pouch. Radiological examination of the proximal cervical region showed rotation of the atlas and the presence of a large bone fragment dorsal to the guttural pouches. Occipital condyle fracture with delayed onset cranial nerve paralysis was diagnosed. Delayed onset cranial nerve paralysis causing dysphagia might be a distinguishable sign of OCF in horses. Delayed onset dysphagia after head injury should prompt equine clinicians to evaluate the condition of the atlanto-occipital articulation and skull base., (© 2019 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine.)

Background: The periesophageal vagus nerve plexus controls the kinetics of the stomach, digestive tract, and gallbladder, and catheter ablation of atrial fibrillation (AF) can cause vagus nerve injury (VNI). We sought to clarify the incidence, clinical course, and anatomical factors related to periesophageal VNI., Methods: The present study included 257 consecutive patients with AF (mean age, 62±11 years) who underwent catheter-based pulmonary vein isolation. With 64-slice computed tomographic images, the left atrium (LA)-esophageal contact length, LA diameter, and distances between each mediastinal structure were compared between patients with VNI and those without VNI., Results: VNI occurred in 5 patients (1.9%), gastric hypomotility in 3 patients, and acalculous cholecystitis in 2 patients, within 3 days after ablation, and all patients recovered completely within 2 weeks. Compared with patients without VNI, those with VNI more frequently underwent ablation at the mitral isthmus (p=0.03) and inside the coronary sinus (p=0.03). On computed tomographic images, the esophagus was closer to the aorta than to the spine in 67% of patients and was defined as an aorta-sided esophagus. In patients with VNI, the distance from the LA to the spine or the descending aorta (in patients with an aorta-sided esophagus) was shorter (p=0.03), and the transverse LA-esophageal contact length was longer (p=0.01)., Conclusion: Acalculous cholecystitis, as well as gastric hypomotility, can develop as a result of periesophageal VNI in patients undergoing AF ablation. The anatomical relationships among the LA, esophagus, spine, and descending aorta may influence the occurrence of VNI.

A 39-year-old male, with a history of multiple suicidal attempts and psychiatric pathology, a professional lumberjack, was found dead at the meadow with his throat cut and a chainsaw beside him. Autopsy revealed that all physical injuries were confined to the head, neck and left shoulder. Two major (long and wide) wounds were found and documented on both sides of the neck and head. A wound on the posterior and right lateral side of his neck and head was noted. Medical examiner noted an irregular rupture on the posterior-right side of the atlanto-occipital joint with impaired bone, but without any damage on the spinal cord. Another gaping cut was noted in the lower part on the left lateral side of his neck. Medical examiner noted that muscles of the left side of the neck, left common carotid artery, left internal jugular vein and left vagus nerve were completely cut off. The body of the C5 and C6 vertebra, with the spinal cord at that level, was completely cut. Also, there were multiple linear and striped parallel abrasions on the outer side of the left shoulder and one abrasion on the left lateral side of the neck. The conclusion of inquiries was "suicide by chainsaw"., (Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)

Vagal nerve injury may occur in esophageal and gastric surgeries. The aim of this study was to observe the effects of ghrelin on small intestinal motility upon vagal nerve injury and the possible co-relationship between changes in ghrelin receptor expression in the small intestine and delayed small intestinal transit after vagotomy. The effects of intraperitoneal administration of ghrelin (20, 40 and 80 µg/kg) and the ghrelin receptor antagonist [D-Lys3]-GHRP-6 (1.5 µmol/kg) on small intestinal transit were studied in control and vagotomized rats in vivo. The effects of ghrelin (0.01, 0.1, 0.5, 1.0 and 2.0 µmol/l) on the contraction force of smooth muscle strips from the jejunum were studied in the presence or absence of carbachol (50 nmol/l) and [D-Lys3]-GHRP-6 (10 µmol/l) in vitro. Ghrelin receptor expression was assessed in intestinal muscle layers by means of Western blotting. The results indicated that ghrelin dose-dependently increased small intestinal transit in the control and model rats. In addition, ghrelin enhanced smooth muscle strip contraction induced by carbachol. Ghrelin receptor antagonist [D-Lys3]-GHRP-6 blocked the effect of ghrelin. Ghrelin receptor expression in the small intestinal muscle layers was down-regulated in the vagotomized rats. Down-regulation of growth hormone secretagogue receptor 1a in small intestinal muscle layers, which affected the function of ghrelin, may be one of the mechanisms behind delayed small intestinal transit after vagotomy.

The real ability of OECs provided by olfactory mucosa cultures (OM-OECs) and those from olfactory bulb cultures (OB-OECs) must be better characterized in order to propose their future clinical application. Therefore, we used a lesion of the vagus nerve (VN), which constitutes a severe motor denervation due to long distance of the muscular targets (4.5 cm). We performed a section/anastomosis surgery of the VN, at the third tracheal ring. Then, OM-OECs and OB-OECs were injected in matrigel around the lesion site. Three months after surgery, laryngeal muscle activity, synkinesis phenomena and latency were evaluated by videolaryngoscopy and electromyography recordings. To complete these procedures, axonal morphometric study of the right recurrent nerve was performed to assess axonal regrowth and tracking of green fluorescent protein positive cells was performed. Recurrent nerve is the motor branch innervating the laryngeal muscles, and is located distally to the lesion, near the muscular targets (0.7 cm). These analyses permitted to compare the ability of these two populations to improve functional recovery and axonal regrowth. Our results show that, OM-OECs improved electrical muscular activity and nervous conduction with significant tissue healing but induced aberrant movement and poor functional recovery. In contrast, OB-OECs induced a partial functional recovery associated with an increase in the number of myelinated fibers and nervous conduction. Our study suggests that, as recently reported in a microarray study, OM-OECs and OB-OECs express different properties. In particular, OM-OECs could regulate inflammation processes and extracellular matrix formation but have a poor regeneration potential, whereas, OB-OECs could improve functional recovery by inducing targeted axonal regrowth., (Copyright © 2010 Elsevier Inc. All rights reserved.)