Abstract
HYPOTHESIS SIGNIFICANT: Cochlear implant (CI) insertion trauma, as evidenced by fracture of the osseous spiral lamina (OSL), is associated with localized "dead zones" and focal spiral ganglion neuron (SGN) loss.
BACKGROUND: Hearing and structure preservation approaches to CI insertion aim to minimize trauma and preserve residual SGNs. In cases of significant insertion trauma, peripheral axons running through the bony OSL inherently become damaged if the OSL is fractured. The current investigation sought to determine if the relative location of OSL fracture was associated with focal areas of SGN loss.
METHODS: Five adult ears from the Mass Eye and Ear Otopathology Laboratory were identified with OSL fractures. When available, contralateral ears were also analyzed for comparison. Digitized e-Slides were used to create 3D cochlear reconstructions, and a coordinate system relative to the round window allowed for % distance along Rosenthal canal (RC) assignment of SGNs and OSL fracture locations. Abrupt changes in SGN density, defined as a drop >50% within a 5% segment along RC were used as criteria for a significant and focal SGN loss. Insertion trauma in the form of electrode translocation and spiral ligament (SL) perforation was also characterized.
RESULTS: OSL fracture lengths ranged from approximately 72 to 109 degrees about the modiolus, with a median fracture length of 75 degrees. Total SGN counts ranged from 16,810 to 22,260. Abrupt and focal drops of >50% in SGN density occurred in all 5 temporal bones with OSL fracture. In 3 of the cases, there were areas of localized "dead zones" at or immediately adjacent to the OSL fracture site, whereas in the remaining 2 cases, drops were seen in various areas across the cochlea. The case with the longest fracture demonstrated nearly a complete loss of neurons apical to the deepest fracture location. Ears with OSL fractures demonstrate a higher number of "dead zones" than the contralateral ears used for comparison, with median values of 3 and 2, respectively. Cases with an OSL fracture, electrode translocation, and SL perforation demonstrated a notably higher number of "dead zones" (median = 3) as compared with ears with only 1 or 2 CI insertional trauma injuries (median = 2).
CONCLUSION: In temporal bones from CI patients, OSL fractures explain some-but not all-of the abrupt SGN loss observed following traumatic CI insertions. Distinct regions of SGN density observed across the length of these cochlea indicate multifactorial processes likely contribute to relative SGN "dead zones."