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A Novel Drug Therapy for Recurrent Laryngeal Nerve Injury Using T‐588
Author(s) -
Mori Yuko,
Shiotani Akihiro,
Saito Koichiro,
Araki Koji,
Ikeda Ken,
Nakagawa Masaya,
Watabe Kazuhiko,
Ogawa Kaoru
Publication year - 2007
Publication title -
the laryngoscope
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.181
H-Index - 148
eISSN - 1531-4995
pISSN - 0023-852X
DOI - 10.1097/mlg.0b013e31805f681f
Subject(s) - medicine , nucleus ambiguus , glial cell line derived neurotrophic factor , nerve growth factor , choline acetyltransferase , neurotrophic factors , anesthesia , recurrent laryngeal nerve , neuroprotection , vagus nerve , nerve injury , pharmacology , acetylcholine , central nervous system , medulla oblongata , receptor , thyroid , stimulation
Objectives/Hypothesis: We have previously shown that gene therapy using Insulin‐like growth factor (IGF)‐I, glial cell line‐derived neurotrophic factor (GDNF), and brain‐derived neurotrophic factor (BDNF), or a combination of these trophic factors, is a treatment option for recurrent laryngeal nerve (RLN) palsy. However, there remain some difficulties preventing this option from becoming a common clinical therapy for RLN injury. Thus, we need to develop novel treatment option that overcomes the problems of gene therapy. R(—)‐1‐(benzothiophen‐5‐yl)‐2‐[2‐N,N‐diethylamino]ethoxy]ethanol hydrochloride (T‐588), a synthetic compound, is known to have neuroprotective effects on neural cells. In the present study, the possibility of new drug treatments using T‐588 for RLN injury was assessed using rat models. Study Design: Animal study. Methods: Animals were administered T‐588 for 4 weeks. The neuroprotective effects of T‐588 administration after vagal nerve avulsion and neurofunctional recovery after recurrent laryngeal nerve crush were studied using motoneuron cell counting, evaluation of choline acetyltransferase immunoreactivity, the electrophysiologic examination, and the re‐mobilization of the vocal fold. Results: T‐588 administration successfully prevented motoneuron loss and ameliorated the choline acetyltransferase immunoreactivity in the ipsilateral nucleus ambiguus after vagal nerve avulsion. Significant improvements of motor nerve conduction velocity of the RLN and vocal fold movement were observed in the treatment group when compared to controls. Conclusion: These results indicate that oral administration of T‐588 might be a promising therapeutic option in treating peripheral nerve injury.