1987
DOI: 10.1007/bf00458549
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Pathological findings in the human auditory system following long-standing gentamicin ototoxicity

Abstract: The clinical, audiovestibular and histopathological findings in a patient who suffered from a long-standing gentamicin-induced deafness are reported. In both temporal bones, the organ of Corti was completely absent, with only a few nerve fibres remaining in the apical part of the cochlea. Regenerative ingrowth of nerve fibers into the area of the degenerative organ of Corti was present apically in both ears. The stria vascularis exhibited considerable degeneration in all turns and loss of microvasculature was … Show more

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Cited by 8 publications
(8 citation statements)
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“…Several views of this relationship can be suggested: (1) that an IHC can release signals that affect the survival of nearby neurons which it does not contact; (2) that, after IHC loss, axons stripped of synaptic contact sprout to connect to surviving IHCs; or (3) that there are signaling interactions among IHCs and supporting cells such that surviving IHCs induce increased synthesis/release of trophic factors (e.g., neurotrophins) from surrounding supporting cells. It is not clear whether any, or all, of these occur; however, there are reports that peripheral axons resprout after hair cell loss from either acoustic overexposure (Strominger et al 1995) or aminoglycoside-induced hair cell death (Backus et al 1987;Tange and Huizing 1980).…”
Section: Primary Vs Secondary Degenerationmentioning
confidence: 96%
“…Several views of this relationship can be suggested: (1) that an IHC can release signals that affect the survival of nearby neurons which it does not contact; (2) that, after IHC loss, axons stripped of synaptic contact sprout to connect to surviving IHCs; or (3) that there are signaling interactions among IHCs and supporting cells such that surviving IHCs induce increased synthesis/release of trophic factors (e.g., neurotrophins) from surrounding supporting cells. It is not clear whether any, or all, of these occur; however, there are reports that peripheral axons resprout after hair cell loss from either acoustic overexposure (Strominger et al 1995) or aminoglycoside-induced hair cell death (Backus et al 1987;Tange and Huizing 1980).…”
Section: Primary Vs Secondary Degenerationmentioning
confidence: 96%
“… 17–31 However, aminoglycoside ototoxicity provides the majority of examples of human temporal bone, including patients treated with streptomycin, 15,17–20 neomycin, 10,15,18,21,22 kanamycin, 18,20,23–28 amikacin, 9,10 and gentamicin. 9,10,12,15,29–32 In addition, there are many other descriptions of patients who were given combinations of ototoxic medications, and descriptions of tobramycin effects are among these. 9,10,12 …”
Section: Introductionmentioning
confidence: 99%
“…Hearing damage associated with aminoglycoside use can include permanent hearing loss and tinnitus secondary to the degradation of sensorineural hair cells of the cochlea and/ or vestibule. Damage to cochlear hair cells is thought to be mediated by oxidative stress, starting at the base where highfrequency sounds are decoded and advancing to the apex 6,8,13,14,15 .…”
Section: Discussionmentioning
confidence: 99%
“…These agents are cost-effective and widely used in lowand middle-income countries 2,3 . Yet, aminoglycoside use for the treatment of MDR-TB is associated with ototoxicity in 5-64% in cases [3][4][5][6][7][8][9][10][11] . Ototoxicity can produce hearing loss and associated psychosocial changes that negatively affect quality of life 12 .…”
Section: Introductionmentioning
confidence: 99%