Histopathology of Human Temporal Bone After Cochlear Implantation

Educational Objectives

The goal of this program is  to reduce the negative effects of cochlear implantation. After hearing and assimilating this program, the clinician will be better able to:

1. Explain the negative effects of cochlear implantation on the cochlea and spiral ganglion cells.

2. Identify techniques to reduce the insertional trauma and loss of spiral ganglion cells associated with cochlear implantation.

Summary

Histopathologic studies of cochlear implantation (CI): insertion of electrode array during procedure causes immediate damage to inner ear and, over time, additional changes that interfere with neuronal stimulation; animal temporal bones (TBs) — animal models of CI allow control over individual variability, cause of deafness, and surgical techniques, but extrapolation of findings to humans not necessarily valid; cadaveric implants — study of human TBs subject to CI after death allows for differentiation of insertional trauma from existing damage, but long-term inflammatory and degenerative changes in remaining spiral ganglion cells (SGC) cannot be studied; donated human TBs from patients who underwent CI during life — offer best way to evaluate long-term deleterious effects of CI on cochlea, as well as how design of electrode or route of insertion may limit or reverse damage

Effect of CI on cochlea: insertional trauma — present in all TBs at site of cochleostomy, with damage to spiral ligament and stria vascularis (particularly ascending limb of basal turn); translocation of electrodes from scala tympani to scala vestibuli or reverse present in 37% of TBs; potential for disruption of spiral lamina, as well as Reissner and basilar membranes; fibrous tissue, new bone formation, and lymphocytic infiltration present at cochleostomy site and in area surrounding electrode; inflammatory response — foreign body granulomatous reaction to electrode (including lymphocytic and foreign body giant cell infiltration) present in 96% of 28 TBs; eosinophilic infiltration (suggesting allergic reaction to electrode) seen in 25%; inflammatory response significantly greater proximal to cochleostomy, but no correlation between duration of CI use and severity of inflammation

Effect of CI on SGC: SGC key component of electrical stimulation of brain and considered target of stimulation of cochlear implants; segments of Rosenthal canal differentially affected — electrode array typically stimulates first 3 of 4 segments (segment I, basal turn; segment IV, apical segment); interaural comparison of 22 TBs from 11 patients after unilateral CI revealed significant decrease in total and apical segment SGC count on side of implant, but no decrease in 3 ipsilateral basal segments where electrode present (suggests protective effect of chronic electric stimulation); bipolar vs monopolar stimulation — within-subject comparison of 52 TBs from 26 patients (16 bipolar and 10 monopolar) showed segmental and total SGC counts lower on side of implant, regardless of mode of stimulation; however, in patients who received bipolar stimulation, difference between SGC counts in implanted vs unimplanted side lower in first 3 basal segments (electrode present) than in apical segment (no electrode); suggests that protective effect on SGC derives from bipolar but not monopolar stimulation

Importance of residual SGC: higher number of residual SGC after CI assumed to result in higher word recognition score (WRS); however, studies of patients with unilateral CI show negative or no correlation between residual SGC count and WRS; in patients with similar number of SGC, WRS varies from 0% to 50%; number of residual SGC one of many clinical variables that affect word recognition after CI; study design — all previous human studies compared SGC counts and WRS across implanted ears of different subjects without sufficient matching for other variables (eg, etiology of deafness, cognitive ability, age); data show residual SGC counts vary substantially across etiologies of deafness (despite similar level of hearing loss), even within diagnostic subgroups; however, one ear of patient may serve as appropriate control for other ear; similar number of SGC present in matched TBs from each patient, perhaps because of common etiology of deafness and similar hearing thresholds; reassessment of performance — in study of 6 patients with bilateral CI, difference in SGC count across ears highly positively correlated with difference in WRS across ears

Factors that influence survival of SGC: new tissue formation — residual SGC counts negatively correlated with new bone formation and growth of fibrous tissue in cochlea (more prominent at basal turn of cochlea segments I and II, cochleostomy site, and ascending basal turn, where insertional trauma more severe; design of electrode affects pattern of fibrosis — capsule of fibrous tissue that surrounds full-banded, straight electrodes thin and evenly distributed, while partially banded perimodiolar (precurved) electrodes induce formation of asymmetric capsule (thicker on modiolar side of electrode); thicker fibrous capsule may increase impedance (resistance of current) targeting modiolus or SGC; impedance nonsignificantly higher in patients implanted with perimodiolar electrode; perimodiolar electrodes caused more severe trauma to cochlea than did straight electrodes; phenomenon attributed to larger diameter (1.1 mm vs 0.6 mm)

Questions and answers: alternate avenues for insertion of electrode — cochleostomy most common in archived human TB specimens; however, insertion through round window thought to cause less trauma and new bone formation than cochleostomy; is lack of correlation between SGC and WRS related to negative effect of trauma on basilar membrane — SGC target of electrical stimulation, so disruption to other structures should not affect performance; however, all cells interlinked, so damage to basilar membrane may decrease number of residual hair cells, reducing sensory input to SGC and causing atrophy

Readings

Ishai R et al: The pattern and degree of capsular fibrous sheaths surrounding cochlear electrode arrays. Hear Res 2017 May;348:44-53; Kamakura T, Nadol JB Jr: Correlation between word recognition score and intracochlear new bone and fibrous tissue after cochlear implantation in the human. Hear Res 2016 Sep;339:132-41; Khan AM et al: Is word recognition correlated with the number of surviving spiral ganglion cells and electrode insertion depth in human subjects with cochlear implants? Laryngoscope 2005 Apr;115(4):672-7; Khan AM et al: Effect of cochlear implantation on residual spiral ganglion cell count as determined by comparison with the contralateral nonimplanted inner ear in humans. Ann Otol Rhinol Laryngol 2005 May;114(5):381-5; Nadol JB Jr et al: Histopathology of cochlear implants in humans. Ann Otol Rhinol Laryngol 2001 Sep;110(9):883-91; Seyyedi M et al: Interaural comparison of spiral ganglion cell counts in profound deafness. Hear Res 2011 Dec;282(1-2):56-62; Seyyedi M et al: Effect of monopolar and bipolar electric stimulation on survival and size of human spiral ganglion cells as studied by postmortem histopathology. Hear Res 2013 Aug;302:9-16; Seyyedi M et al: Within-subject comparison of word recognition and spiral ganglion cell count in bilateral cochlear implant recipients. Otol Neurotol 2014 Sep;35(8):1446-50; Seyyedi M, Nadol JB Jr: Intracochlear inflammatory response to cochlear implant electrodes in humans. Otol Neurotol 2014 Oct;35(9):1545-51.

Disclosures

For this program, the following has been disclosed: Dr. Seyyedi reported nothing to disclose. The planning committee reported nothing to disclose.

Acknowledgements

Dr. Seyyedi was recorded at the 16th Annual Porubsky Symposium, held June 8-9, 2018, in Augusta, GA, and presented by the Augusta Otolaryngology Educational Foundation, Medical College of Georgia at Augusta University. For information on future CME activities from this sponsor, please visit augusta.edu/pace/healthcare/medicine. The Audio Digest Foundation thanks the speakers and sponsors for their cooperation in the presentation of this program.

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Audio Digest Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's (ANCC's) Commission on Accreditation. Audio Digest Foundation designates this activity for 0 CE contact hours.

Lecture ID:

OT511903

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.