title: Temporal pattern of cochlear nerve degeneration following compression injury: a quantitative experimental observation.
abstract: OBJECTIVE
  It has been empirically recognized that the cochlear nerve is highly vulnerable to traumatic stress resulting from surgical procedures; therefore, careful manipulation of the cochlear nerve is mandatory in preventing trauma-induced hearing loss during cerebellopontine angle (CPA) surgery. There is, however, no precise knowledge about the temporal pattern of cochlear nerve degeneration following trauma. This study was performed to determine the temporal pattern of injury that occurs after cochlear nerve trauma, knowledge of which is indispensable not only to neurosurgeons but also to all those who manage lesions involving the cochlear nerve.
  
  
  METHODS
  Right suboccipital craniectomies were performed in groups of rats with the aid of a surgical microscope, and the seventh and eighth cranial nerve trunks were identified at the internal auditory meatus. The cochlear nerve was quantifiably compressed while compound action potentials of the cochlear nerve were monitored and recorded. Following injury, one group of rats was killed for histological examination at the end of each week for 4 weeks. Data from this study disclosed that the degeneration of the compressed cochlear nerve progressed in a relatively rapid manner and was complete within 1 week after the insult. The main pathophysiological mechanisms responsible for cochlear neuronal death in this experimental setting appeared to be necrosis, and an apoptotic mechanism seemed to play a subsidiary role.
  
  
  CONCLUSIONS
  Accurate knowledge about the temporal profile of trauma-induced cochlear nerve degeneration is closely linked with the problem of the therapeutic time window. The results of the present study indicated that any measures to ameliorate cochlear nerve degeneration following trauma should be started as early as possible (within 1 week) after an injury.
authors.affiliation: Department of Neurosurgery, Hirosaki University School of Medicine, Japan.
authors.forename: Norihito
authors.initials: N
authors.lastname: Shimamura
authors.forename: Tetsuji
authors.initials: T
authors.lastname: Sekiya
authors.forename: Akinori
authors.initials: A
authors.lastname: Yagihashi
authors.forename: Shigeharu
authors.initials: S
authors.lastname: Suzuki
mesh_terms: D000818:Animals; D017209:Apoptosis; D018450:Disease Progression; D005072:Evoked Potentials, Auditory; D008297:Male; D009336:Necrosis; D009408:Nerve Compression Syndromes / Q000150:complications / Q000473:pathology*; D009410:Nerve Degeneration / Q000209:etiology / Q000473:pathology*; D009475:Neurons, Afferent / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013136:Spiral Ganglion / Q000473:pathology; D000160:Vestibulocochlear Nerve Diseases / Q000209:etiology / Q000473:pathology*