Olfactory-ensheathing cells promote physiological repair of injured recurrent laryngeal nerves and functional recovery of glottises in dogs.

The aim of this study was to investigate whether the transplantation of olfactory-ensheathing cells (OECs) could physiologically repair severely injured recurrent laryngeal nerve (RLN) in dogs. Adult Beagle dogs were surgically introduced with a 10-mm defect in the left RLN and transplanted with a nerve guide (NEUROLAC) containing dog olfactory mucosa-olfactory-ensheathing cells (OM-OECs) in matrigel. The effects of OM-OECs on the morphology, histology, and electrophysiology of the injured RLNs, glottis movement, and voice acoustics were comparatively studied. Two months after transplantation, the normal dogs (group N) had intact left RLNs that contained axons well organized as bundles, transmitted action potentials of high amplitudes without latent phases, and modulated glottis movement to produce normal voices. The RLN-damaged dogs transplanted with OM-OECs (group CTT) had pieces of nerves regenerated in the place of the defects, which contained fewer axons scattered in the internal nerve membrane and wrapped peripherally by the connective tissue, prevented the distal trunk of the defected RLN from shrinking, transmitted action potentials of lower amplitudes with latent phases, and modulated a slightly impaired glottis movement to produce voices with slight differences compared to the N dogs. The RLN-damaged dogs without OM-OECs (group NC) had no nerves generated at the defective or the damaged area, leading to a shrinkage in the enervated distal nerve trunks; a blockage in nerve pulse transit; a paralysis of the left vocal cords; an impaired glottis movement; and abnormal voices. Transplantation of OM-OECs promoted nerve regeneration, and the recoveries of glottises and voices in dogs with RLN injury.

[The possibilities for the restoration of the laryngeal function: the current state-of-the-art]. / Vozmozhnosti vosstanovleniia funktsii gortani: sovremennyi podkhod.

The restoration of the functional competence of the larynx following bilateral laryngeal nerve damage and vocal fold paralysis is a serious challenge for the surgeon that has thus far no satisfactory solution. Physiological re-innervation that occurs naturally with time is non-selective and, in the majority of the cases, leads to synkinesis. Laryngeal pacing achieved with the application of the implantable microchips appears to be a promising approach. The animal experiments have demonstrated the possibility of successful restoration of all the functions of the larynx by means of laryngeal pacing but simultaneously revealed a number of technical issues that have to be addressed if the further progress in this field is to be achieved including the choice of the proper materials for implantation, solution of problems pertaining to the neuromuscular mapping during pacer implantation, etc.). The results of the first prospective clinical trial involving the human patients gave evidence suggesting that the laryngeal electrostimulation technology is both safe and efficient. Nevertheless, further investigations and modification of the method are needed before it can be recommended for the wider application in the routine clinical practice.

Changes in neurotrophic factors of adult rat laryngeal muscles during nerve regeneration.

Injury to the recurrent laryngeal nerve (RLN) leads to the loss of ipsilateral laryngeal fold movement, with dysphonia, and occasionally dysphagia. Functional movement of the vocal folds is never restored due to misrouting of regenerating axons to agonist and antagonist laryngeal muscles. Changes of neurotrophic factor expression within denervated muscles occur after nerve injury and may influence nerve regeneration, axon guidance and muscle reinnervation. This study investigates the expression of certain neurotrophic factors in the laryngeal muscles during the course of axonal regeneration using RT-PCR. The timing of neurotrophic factor expression was correlated to the reinnervation of the laryngeal muscles by motor axons. Nerve Growth Factor (NGF), Brain-Derived Neurotrophic Factor (BDNF) and Netrin-1 (NTN-1) increased their expression levels in laryngeal muscles after nerve section and during regeneration of RLN. The upregulation of trophic factors returned to control levels following regeneration of RLN. The expression levels of the neurotrophic factors were correlated with the innervation of regenerating axons into the denervated muscles. The results suggest that certain neurotrophic factor expression is strongly correlated to the reinnervation pattern of the regenerating RLN. These factors may be involved in guidance and neuromuscular junction formation during nerve regeneration. In the future, their manipulation may enhance the selective reinnervation of the larynx.

Intraoperative neural monitoring in thyroid cancer surgery.

BACKGROUND: Intraoperative neural monitoring (IONM) has increasingly garnered the attention of the surgeons performing thyroid and parathyroid surgery around the world. Current studies suggest a majority of general and head and neck surgeons utilize neural monitoring in their thyroid surgical case load in both the US and Germany. PURPOSE: We aim to present an up-to-date review of the application of IONM specifically focusing on its utility in thyroid cancer surgery. Neural monitoring is discussed particularly as it relates to neural prognosis, the issues of staged thyroid surgery for thyroid cancer, and new horizons in the monitoring of the superior laryngeal nerve (SLN) and prevention of neural injury through continuous vagal neural monitoring. CONCLUSION: IONM, as it relates to thyroid surgery, has obtained a widespread acceptance as an adjunct to the gold standard of visual nerve identification. The value of IONM in prognosticating neural function and in intraoperative decision making regarding proceeding to bilateral surgery is also well-known. Initial data on recent extensions of IONM in the form of SLN monitoring and continuous vagal nerve monitoring are promising. Continuous vagal nerve monitoring expands the utility of IONM by providing real-time electrophysiological information, allowing surgeons to take a corrective action in impending neural injury.

Quantity and three-dimensional position of the recurrent and superior laryngeal nerve lower motor neurons in a rat model.

OBJECTIVES: We sought to elucidate the 3-dimensional position and quantify the lower motor neurons (LMNs) of the recurrent laryngeal nerve (RLN) and the superior laryngeal nerve (SLN) in a rat model. Quantification and mapping of these neurons will enhance the usefulness of the rat model in the study of reinnervation following trauma to these nerves. METHODS: Female Sprague-Dawley rats underwent microsurgical transection of the RLN, the SLN, or both the RLN and SLN or sham surgery. After transection, either Fluoro-Ruby (FR) or Fluoro-Gold (FG) was applied to the proximal nerve stumps. The brain stems were harvested, sectioned, and examined for fluorolabeling. The LMNs were quantified, and their 3-dimensional position within the nucleus ambiguus was mapped. RESULTS: Labeling of the RLN was consistent regardless of the labeling agent used. A mean of 243 LMNs was documented for the RLN. The SLN labeling with FR was consistent and showed a mean of 117 LMNs; however, FG proved to be highly variable in labeling the SLN. The SLN LMNs lie rostral and ventral to those of the RLN. In the sham surgical condition, FG was noted to contaminate adjacent tissues--in particular, in the region of the SLN. CONCLUSIONS: Fluorolabeling is an effective tool to locate and quantify the LMNs of the RLN and SLN. The LMN positions and counts were consistent when FR was used in labeling of either the RLN or the SLN. Fluoro-Gold, however, because of its tendency to contaminate surrounding structures, can only be used to label the RLN. Also, as previously reported, the SLN LMNs lie rostral and ventral to those of the RLN. This information results in further clarification of a rat model of RLN injury that may be used to investigate the effects of neurotrophic factors on RLN reinnervation.