title: Facial nerve injury caused by vestibular Schwannoma compression: severity and adaptation to maintain normal clinical facial function.
abstract: OBJECTIVE
  To assess facial nerve injury caused by vestibular Schwannoma compression and the adaptive ability of the nerve/muscle complex to maintain normal clinical facial function.
  
  
  METHODS
  Prospective study.
  
  
  METHODS
  Tertiary referral centre.
  
  
  METHODS
  Thirty-four patients undergoing translabyrinthine resection of vestibular schwannoma.
  
  
  METHODS
  Diagnostic.
  
  
  METHODS
  Facial nerve action potential (FNAP) amplitude recorded at the second genu enables direct assessment of motoneuron function. Comparison of FNAP amplitudes to stimulation proximal and distal to tumor compression allows calculation of motoneuron conduction block across the site of tumor compression. Recordings performed before tumor dissection from the facial nerve reflects nerve injury caused by vestibular Schwannoma compression alone. Comparison of compound muscle action potential (CMAP) amplitudes to stimulation proximal and distal to tumor compression measures motoneuron conduction block and compensatory collateral sprouting at the nerve/muscle interface. Comparison of FNAP and CMAP data demonstrates the extent of collateral sprouting, which helps maintain normal clinical facial function.
  
  
  RESULTS
  Normal clinical facial function is maintained when only 10% of functioning motoneurons are active. The facial nerve is highly susceptible to tumor compression with significant motoneuron injury occurring with all sizes of tumors. Motoneuron injury correlates with tumor size but with exceptions. Collateral sprouting maintains muscle function despite severe motoneuron injury. There is a significant decrease in muscle function when >80% of functioning motoneurons are in conduction block.
  
  
  CONCLUSIONS
  The facial nerve is highly susceptible to vestibular Schwannoma compression. Collateral sprouting of active functioning motoneurons reinnervate denervated muscle fibers so maintaining muscle function and therefore clinical facial function.
authors.affiliation: University Department of Otolaryngology, Manchester Royal Infirmary, United Kingdom.
authors.forename: P R
authors.initials: PR
authors.lastname: Axon
authors.forename: R T
authors.initials: RT
authors.lastname: Ramsden
mesh_terms: D000222:Adaptation, Physiological; D000328:Adult; D000368:Aged; D001933:Brain Stem / Q000502:physiology; D003390:Cranial Nerve Neoplasms / Q000150:complications*; D004428:Ear Neoplasms / Q000150:complications* / Q000601:surgery; D004558:Electric Stimulation / Q000379:methods; D004594:Electrophysiology; D005071:Evoked Potentials / Q000502:physiology; D005152:Facial Muscles / Q000502:physiology; D020220:Facial Nerve Injuries / Q000175:diagnosis* / Q000209:etiology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009046:Motor Neurons / Q000502:physiology; D009408:Nerve Compression Syndromes / Q000175:diagnosis*; D009464:Neuroma, Acoustic / Q000150:complications* / Q000601:surgery; D011446:Prospective Studies; D012720:Severity of Illness Index