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Free Radicals in ENT Pathology pp 395–421Cite as

Loss of Residual Hearing Initiated by Cochlear Implantation: Role of Inflammation-Initiated Cell Death Pathways, Wound Healing and Fibrosis Pathways, and Potential Otoprotective Therapies

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Abstract

Cochlear implantation with electrode array insertion, even in the best of surgical hands, can be traumatic, causing the release of pro-inflammatory and apoptotic factors that lead to loss of auditory hair cells that are critical for the retention of a cochlear implant patient’s residual hearing. The chronic inflammatory process following cochlear implantation can lead to cochlear fibrosis and increased cochlear implant (CI) impedance. This can interfere with function of the implant alone or when combined with acoustic stimulation as in electroacoustic stimulation of the auditory system. Less-traumatic surgical techniques have been developed and electrode arrays have been modified to reduce trauma associated with cochlear implantation. In addition, several drug therapies have been shown to reduce postoperative inflammation and conserve residual hearing in animal models of electrode insertion trauma-induced hearing loss. These drug therapies show promise for future use in CI patients, where conservation of residual hearing is a goal and these promising therapies need to be tested in clinical trials. Preserving residual low-frequency hearing in CI patients may provide improved speech perception in quiet and noise and enhanced music perception compared to CI patients that lose residual audition. Despite conservation of residual hearing with more advanced surgical techniques and low trauma electrode designs, residual native auditory function continues to deteriorate years after surgery. Future trends of cochlear implantation will likely focus on drug-eluting electrodes and longer less-traumatic electrodes that can compensate for a loss of residual hearing many years post-implantation.

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Abbreviations

ABR:

Auditory brainstem response

AIF:

Apoptosis-inducing factor

Apaf-1:

Apoptotic peptidase-activating factor 1

BAX:

Bcl-2-associated X protein

BID:

BH3 Interaction domain

BMPs:

Bone morphogenic proteins

CI:

Cochlear implant

Cyt. C :

Cytochrome C

DIABLO:

Direct Inhibition of apoptosis-binding protein with low pI

DISC:

Death-inducing signaling complex

D-JNKI-1:

D-JNK inhibitor peptide 1

DR:

Death receptor

DR3:

Death receptor three

DR4:

Death receptor four

DR5:

Death receptor five

DXM:

Dexamethasone

EAS:

Electroacoustic stimulation

EIT:

Electrode insertion trauma

EMT:

Epithelial to mesenchymal cell transition

Endo-G:

Endonuclease G

EP:

Endolymphatic potential

ERK:

Extracellular signal regulated kinase

FADD:

Fas-associated death domain

GCR:

Glucocorticoid receptor

HC:

Hair cells

IAPs:

Inhibitors of apoptosis

IHC:

Inner hair cell

IL-1β:

Interleukin one beta

IL-6:

Interleukin six

iNOS:

Inducible nitric oxide synthase

JNKs:

c-JUN N-terminal kinases

L-NAC:

l-N-acetylcysteine

MAPKs:

Mitogen-activated protein kinases

NFκB:

Nuclear factor kappa B

NT-3:

Neurotrophin-3

OC:

Organ of corti

OHC:

Outer hair cell

Omi/HtrA2:

Mammalian homology of bacterial high temperature requirement protein

PI3K:

Phosphatidylinositol 3-kinase

Ppy/pTS/NT-3:

Polypyrrole/para-toluene sulfonate containing neurotrophin-3

ROS:

Reactive oxygen species

SG:

Spiral ganglion

SIBS:

Styrene–isobutylene–styrene

Smac:

Second mitochondria-derived activator of caspases

tBID:

Truncated BID

TGFβ:

Transforming growth factor beta

TNF α:

Tumor necrosis factor alpha

TNFR1:

Tumor necrosis factor receptor 1

TRADD:

TNFR1-associated death domain

TRAIL-R1:

TNF-related apoptosis-inducing ligand receptor 1

TRAIL-R2:

TNF-related apoptosis-inducing ligand receptor 2

TRAMP:

TNF-like receptor apoptosis-mediating protein

XIAP:

X-linked inhibition of apoptosis proteins

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Acknowledgment

The writing of this chapter was supported by the following grants: MED-EL Hearing Devices Company, Innsbruck, Austria to T.R.V. and E.B.; The American Hearing Research Foundation to E.B. and C.T.D.

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    Authors and Affiliations

    1. Department of Otolaryngology, University of Miami Ear Institute, University of Miami Miller School of Medicine, 1600 NW 10th Avenue, RMSB 3160, Miami, FL, 33136, USA

      Esperanza Bas Ph.D., Christine T. Dinh M.D., Rosemary Ojo M.D., Adrien A. Eshraghi M.D. & Thomas R. Van De Water Ph.D.

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    1. Esperanza Bas Ph.D.
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    2. Christine T. Dinh M.D.
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    3. Rosemary Ojo M.D.
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    Correspondence to Thomas R. Van De Water Ph.D. .

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    Editors and Affiliations

    1. Cochlear Signaling & Tissue Engin., University of Michigan Kresge Hearing Research Institute, Ann Arbor, Michigan, USA

      Josef Miller

    2. Dept of Speech , Lang & Hearing Sci, Univ of Florida Health Sciences Center, Gainesville, Florida, USA

      Colleen G. Le Prell

    3. Div . of Otolaryngology Head & Neck Surgery, SIU School of Medicine, Springfield, Illinois, USA

      Leonard Rybak

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    Bas, E., Dinh, C.T., Ojo, R., Eshraghi, A.A., Van De Water, T.R. (2015). Loss of Residual Hearing Initiated by Cochlear Implantation: Role of Inflammation-Initiated Cell Death Pathways, Wound Healing and Fibrosis Pathways, and Potential Otoprotective Therapies. In: Miller, J., Le Prell, C., Rybak, L. (eds) Free Radicals in ENT Pathology. Oxidative Stress in Applied Basic Research and Clinical Practice. Humana Press, Cham. https://doi.org/10.1007/978-3-319-13473-4_19

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