Intratympanic Steroid Prevents Long-Term Spiral Ganglion Neuron Loss in Experimental Meningitis

Abstract

Intratympanic steroid treatment prevents hearing loss and cochlear damage in a rat model of pneumococcal meningitis. Sensorineural hearing loss is a long-term complication of meningitis affecting up to a third of survivors. Streptococcus pneumoniae is the bacterial species most often associated with a hearing loss. Rats were randomly assigned to 3 treatment groups: a group treated with intratympanic betamethasone and 2 control groups treated with either intratympanic or systemic saline. Treatment was initiated 21 hours after infection and repeated once a day for 3 days. Hearing loss and cochlear damage were assessed by distortion product otoacoustic emissions, auditory brainstem response at 16 kHz, and spiral ganglion neuron density. Fifty-six days after infection, auditory brainstem response showed no significant differences between groups, and distortion product otoacoustic emissions showed significant hearing loss at the low frequencies in animals treated with intratympanic steroid compared with animals treated with systemic saline (p < 0.05; Mann-Whitney test). However, intratympanic steroid significantly increased the number of viable neurons in the spiral ganglion compared with both intratympanic and systemic saline (p = 0.0082 and p = 0.0089; Mann-Whitney test). Histology revealed fibrosis of the tympanic membrane and cavity in steroid-treated animals, which plausibly caused the low-frequency hearing loss. Intratympanic betamethasone treatment prevents long-term spiral ganglion neuron loss in experimental pneumococcal meningitis. This finding is clinically relevant in relation to post-meningitic hearing rehabilitation by cochlear implantation. However, the drug instillation in the middle ear induced local fibrosis and a concurrent low-frequency hearing loss.