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Intratympanic steroid prevents long-term spiral ganglion neuron loss in experimental meningitis

Lise Worsøe1, Christian Thomas Brandt, Søren Peter Lund

  • 1Department of Oto-rhino-laryngology, Head and Neck Surgery, Copenhagen University Hospital Gentofte, Hellerup, Denmark. l_worsoe@hotmail.com

Otology & Neurotology : Official Publication of the American Otological Society, American Neurotology Society [And] European Academy of Otology and Neurotology
|February 12, 2010
PubMed
Abstract

Insights

Intratympanic steroid treatment in rats with pneumococcal meningitis preserved spiral ganglion neurons but caused low-frequency hearing loss due to local fibrosis. This highlights a trade-off in treating meningitis-induced hearing damage.

Area of Science:

  • Otolaryngology
  • Neuroscience
  • Infectious Diseases

Background:

  • Sensorineural hearing loss is a common sequela of meningitis, affecting up to one-third of survivors.
  • Streptococcus pneumoniae is a leading bacterial cause of meningitis-associated hearing loss.
  • Cochlear damage and neuronal loss contribute to post-meningitic hearing impairment.

Purpose of the Study:

  • To evaluate the efficacy of intratympanic steroid treatment in preventing hearing loss and cochlear damage in a rat model of pneumococcal meningitis.
  • To assess the impact of intratympanic betamethasone on spiral ganglion neuron survival and auditory function.
  • To investigate potential adverse effects of intratympanic drug delivery in the context of meningitis.

Main Methods:

  • Rats with pneumococcal meningitis were randomized into three groups: intratympanic betamethasone, intratympanic saline, or systemic saline.
  • Treatment commenced 21 hours post-infection and was administered daily for three days.
  • Auditory function was assessed using distortion product otoacoustic emissions and auditory brainstem response; cochlear damage was evaluated by spiral ganglion neuron density.

Main Results:

  • Intratympanic steroid treatment significantly increased spiral ganglion neuron survival compared to saline controls (p < 0.01).
  • While neuronal loss was prevented, intratympanic steroids resulted in significant low-frequency hearing loss (p < 0.05) compared to systemic saline.
  • Histological analysis revealed tympanic membrane and middle ear cavity fibrosis in steroid-treated animals, likely causing the observed low-frequency hearing deficit.

Conclusions:

  • Intratympanic betamethasone effectively prevents long-term spiral ganglion neuron loss in experimental pneumococcal meningitis.
  • The neuroprotective effect is clinically relevant for hearing rehabilitation strategies, such as cochlear implantation, following meningitis.
  • Local fibrosis and subsequent low-frequency hearing loss are potential side effects of intratympanic drug administration in this model.

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