Local neurotoxins for prevention of laryngeal synkinesis after recurrent laryngeal nerve injury

Bryan R. McRae, John Kincaid, Elisa A. Illing, Kelly K. Hiatt, Jan F. Hawkins, Stacey L. Halum

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Objectives: Persistent vocal fold motion impairment after recurrent laryngeal nerve (RLN) injury is not characteristically due to absent reinnervation, but often results from spontaneous aberrant reinnervation (synkinesis). We administered local neurotoxins to selected laryngeal muscles after RLN injury to determine whether aberrant reinnervation could be selectively inhibited. Methods: Unilateral RLN transection was performed in 24 male rats. Three weeks later, the denervated laryngeal adductor complex was injected with phenol, high- or low-dose vincristine sulfate (VNC), or saline solution. One month later, rat larynges were evaluated via videolaryngoscopy and laryngeal electromyography (LEMG). Larynges from euthanized animals were analyzed via immunofluorescent staining for the presence of reinnervation. Results: One animal that received phenol and 3 animals that received high-dose VNC died of toxicity-related complications. In the surviving neurotoxin-treated animals, videolaryngoscopy showed increased lateralization of the immobile vocal fold. Only 1 phenol-injected rat had adductor complex motor recruitment (score of 3+) with LEMG. The other neurotoxin-treated animals demonstrated an absence of adductor complex reinnervation, with only insertional activity and fibrillations (no motor units/recruitment). Spontaneous ipsilateral abductor reinnervation was not affected by the adductor injections. Conclusions: Low-dose VNC injections appear to be relatively safe and effective in selectively inhibiting spontaneous aberrant reinnervation after RLN injury in an animal model.

Original languageEnglish
Pages (from-to)887-893
Number of pages7
JournalAnnals of Otology, Rhinology and Laryngology
Volume118
Issue number12
StatePublished - Dec 2009

Fingerprint

Synkinesis
Recurrent Laryngeal Nerve Injuries
Neurotoxins
Vincristine
Phenol
Vocal Cords
Electromyography
Larynx
Neurophysiological Recruitment
Laryngeal Muscles
Injections
Sodium Chloride
Animal Models
Staining and Labeling

Keywords

  • Larynx
  • Recurrent laryngeal nerve
  • Synkinesis
  • Vincristine
  • Vocal fold motion impairment
  • Vocal fold paralysis

ASJC Scopus subject areas

  • Otorhinolaryngology

Cite this

McRae, B. R., Kincaid, J., Illing, E. A., Hiatt, K. K., Hawkins, J. F., & Halum, S. L. (2009). Local neurotoxins for prevention of laryngeal synkinesis after recurrent laryngeal nerve injury. Annals of Otology, Rhinology and Laryngology, 118(12), 887-893.

Local neurotoxins for prevention of laryngeal synkinesis after recurrent laryngeal nerve injury. / McRae, Bryan R.; Kincaid, John; Illing, Elisa A.; Hiatt, Kelly K.; Hawkins, Jan F.; Halum, Stacey L.

In: Annals of Otology, Rhinology and Laryngology, Vol. 118, No. 12, 12.2009, p. 887-893.

Research output: Contribution to journalArticle

McRae, Bryan R. ; Kincaid, John ; Illing, Elisa A. ; Hiatt, Kelly K. ; Hawkins, Jan F. ; Halum, Stacey L. / Local neurotoxins for prevention of laryngeal synkinesis after recurrent laryngeal nerve injury. In: Annals of Otology, Rhinology and Laryngology. 2009 ; Vol. 118, No. 12. pp. 887-893.
@article{0d3203606ace413e83fe98f1a52c6ddd,
title = "Local neurotoxins for prevention of laryngeal synkinesis after recurrent laryngeal nerve injury",
abstract = "Objectives: Persistent vocal fold motion impairment after recurrent laryngeal nerve (RLN) injury is not characteristically due to absent reinnervation, but often results from spontaneous aberrant reinnervation (synkinesis). We administered local neurotoxins to selected laryngeal muscles after RLN injury to determine whether aberrant reinnervation could be selectively inhibited. Methods: Unilateral RLN transection was performed in 24 male rats. Three weeks later, the denervated laryngeal adductor complex was injected with phenol, high- or low-dose vincristine sulfate (VNC), or saline solution. One month later, rat larynges were evaluated via videolaryngoscopy and laryngeal electromyography (LEMG). Larynges from euthanized animals were analyzed via immunofluorescent staining for the presence of reinnervation. Results: One animal that received phenol and 3 animals that received high-dose VNC died of toxicity-related complications. In the surviving neurotoxin-treated animals, videolaryngoscopy showed increased lateralization of the immobile vocal fold. Only 1 phenol-injected rat had adductor complex motor recruitment (score of 3+) with LEMG. The other neurotoxin-treated animals demonstrated an absence of adductor complex reinnervation, with only insertional activity and fibrillations (no motor units/recruitment). Spontaneous ipsilateral abductor reinnervation was not affected by the adductor injections. Conclusions: Low-dose VNC injections appear to be relatively safe and effective in selectively inhibiting spontaneous aberrant reinnervation after RLN injury in an animal model.",
keywords = "Larynx, Recurrent laryngeal nerve, Synkinesis, Vincristine, Vocal fold motion impairment, Vocal fold paralysis",
author = "McRae, {Bryan R.} and John Kincaid and Illing, {Elisa A.} and Hiatt, {Kelly K.} and Hawkins, {Jan F.} and Halum, {Stacey L.}",
year = "2009",
month = "12",
language = "English",
volume = "118",
pages = "887--893",
journal = "Annals of Otology, Rhinology and Laryngology",
issn = "0003-4894",
publisher = "Annals Publishing Company",
number = "12",

}

TY - JOUR

T1 - Local neurotoxins for prevention of laryngeal synkinesis after recurrent laryngeal nerve injury

AU - McRae, Bryan R.

AU - Kincaid, John

AU - Illing, Elisa A.

AU - Hiatt, Kelly K.

AU - Hawkins, Jan F.

AU - Halum, Stacey L.

PY - 2009/12

Y1 - 2009/12

N2 - Objectives: Persistent vocal fold motion impairment after recurrent laryngeal nerve (RLN) injury is not characteristically due to absent reinnervation, but often results from spontaneous aberrant reinnervation (synkinesis). We administered local neurotoxins to selected laryngeal muscles after RLN injury to determine whether aberrant reinnervation could be selectively inhibited. Methods: Unilateral RLN transection was performed in 24 male rats. Three weeks later, the denervated laryngeal adductor complex was injected with phenol, high- or low-dose vincristine sulfate (VNC), or saline solution. One month later, rat larynges were evaluated via videolaryngoscopy and laryngeal electromyography (LEMG). Larynges from euthanized animals were analyzed via immunofluorescent staining for the presence of reinnervation. Results: One animal that received phenol and 3 animals that received high-dose VNC died of toxicity-related complications. In the surviving neurotoxin-treated animals, videolaryngoscopy showed increased lateralization of the immobile vocal fold. Only 1 phenol-injected rat had adductor complex motor recruitment (score of 3+) with LEMG. The other neurotoxin-treated animals demonstrated an absence of adductor complex reinnervation, with only insertional activity and fibrillations (no motor units/recruitment). Spontaneous ipsilateral abductor reinnervation was not affected by the adductor injections. Conclusions: Low-dose VNC injections appear to be relatively safe and effective in selectively inhibiting spontaneous aberrant reinnervation after RLN injury in an animal model.

AB - Objectives: Persistent vocal fold motion impairment after recurrent laryngeal nerve (RLN) injury is not characteristically due to absent reinnervation, but often results from spontaneous aberrant reinnervation (synkinesis). We administered local neurotoxins to selected laryngeal muscles after RLN injury to determine whether aberrant reinnervation could be selectively inhibited. Methods: Unilateral RLN transection was performed in 24 male rats. Three weeks later, the denervated laryngeal adductor complex was injected with phenol, high- or low-dose vincristine sulfate (VNC), or saline solution. One month later, rat larynges were evaluated via videolaryngoscopy and laryngeal electromyography (LEMG). Larynges from euthanized animals were analyzed via immunofluorescent staining for the presence of reinnervation. Results: One animal that received phenol and 3 animals that received high-dose VNC died of toxicity-related complications. In the surviving neurotoxin-treated animals, videolaryngoscopy showed increased lateralization of the immobile vocal fold. Only 1 phenol-injected rat had adductor complex motor recruitment (score of 3+) with LEMG. The other neurotoxin-treated animals demonstrated an absence of adductor complex reinnervation, with only insertional activity and fibrillations (no motor units/recruitment). Spontaneous ipsilateral abductor reinnervation was not affected by the adductor injections. Conclusions: Low-dose VNC injections appear to be relatively safe and effective in selectively inhibiting spontaneous aberrant reinnervation after RLN injury in an animal model.

KW - Larynx

KW - Recurrent laryngeal nerve

KW - Synkinesis

KW - Vincristine

KW - Vocal fold motion impairment

KW - Vocal fold paralysis

UR - http://www.scopus.com/inward/record.url?scp=74549210131&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=74549210131&partnerID=8YFLogxK

M3 - Article

C2 - 20112524

AN - SCOPUS:74549210131

VL - 118

SP - 887

EP - 893

JO - Annals of Otology, Rhinology and Laryngology

JF - Annals of Otology, Rhinology and Laryngology

SN - 0003-4894

IS - 12

ER -