LAUSR

I read with great interest the article by Islamoglu et al. entitled “Single-sided deafness after sudden hearıng loss: late effect on cochlear nerve size” [1]. I have some concerns about the study’s conclusion that I would like to address. Their study compared the diameter of the cochlear nerve (CN) of the affected ear vs. the contralateral control (nonaffected) ear among patients with single-sided deafness (SSD) of at least 5 years’ duration. They used routine internal auditory canal directed high-resolution 3D-T2 Space constant magnetic resonance imaging (MRI) scanning, which is performed for every sudden hearing loss to exclude a vestibular schwannoma. Having found no significant difference between the normal and deaf ears of the subjects in terms of CN vertical diameter, horizontal diameter, and area, the authors speculated that “This result may show no significant loss of spiral ganglion cells over the years in terms of cochlear implant success.” The authors based this speculation on the study of Nadol and Xu [2] who concluded that “There is a significant positive correlation between the remaining spiral ganglion cell counts and the diameters of the cochlear, vestibular, and cochleovestibular nerves.” However, only three patients in the report by Nadol and XU had sudden hearing loss, while the others had many other pathologies, some of which were neural and not sensory (e.g., cerebellopontine angle tumors). Since the primary insult in sudden hearing loss is thought to be sensory and not neural, it is difficult to draw any conclusions from Nadol and Xu’s study which was conducted on multiple pathologies. A recent histologic study by Ungar et al. [3] demonstrated that there is a decay of spiral ganglion cell count (SGCC) in ears with sudden hearing loss as a function of time. The essential point here is that auditory neurons may survive after degeneration of the cochlea and spiral ganglion cells [4]. Since the process of spiral ganglion cell decay is chronic, and since the soma dies before its axon, it is possible that the CN diameter will still be normal, even though the SGCC is reduced. Contemporary pre-mortem methodologies, such as MRI and auditory brainstem response (ABR), are not yet capable of counting SGCC, without which cochlear implants would be contraindicated, and, as such, this casts doubts on the conclusions reached by Islamoglu et al. It would be interesting to compare the pre-mortem CN diameter as measured on MRI and the ABR to the postmortem SGCC as counted on light microscopy in patients with long-standing unilateral sensorineural hearing losses. Those results might give us some greater clarification of the clinical implications of the CN diameter on cochlear implantation.