Number Of Spiral Ganglion Cells Research Articles

Meta-Analysis-Correlation between Spiral Ganglion Cell Counts and Speech Perception with a Cochlear Implant.

The presence of spiral ganglion cells (SGCs) is widely accepted to be a prerequisite for successful speech perception with a cochlear implant (CI), because SGCs provide the only known conduit between the implant electrode and the central auditory system. By extension, it has been hypothesized that the number of SGCs might be an important factor in CI outcomes. An impressive body of work has been published on findings from the laborious process of collecting temporal bones from CI users and counting the number of SGCs to correlate those numbers with speech perception scores, but the findings thus far have been conflicting. We performed a meta-analysis of all published studies with the hope that combining existing data may help us reach a more definitive conclusion about the relationship between SGC count and speech perception scores in adults.

Influence of cochlear parameters on the current practice in cochlear implantation : Development of aconcept for personalized medicine.

Since the introduction of cochlear implants into clinical routine, the interest in measuring cochlear parameters, particularly the cochlear duct length (CDL) has increased, since these can have an influence on the correct selection of the electrode. On the one hand, coverage of an optimal frequency band is relevant for agood audiological result, and on the other hand, cochlear trauma due to too deep insertion or displacement of the electrode must be avoided. Cochlear implants stimulate the spiral ganglion cells (SGC). The number of SGC and particularly their distribution can also have an influence on the function of acochlear implant. In addition, the frequency assignment of each electrode contact can play adecisive role in the postoperative success, since the frequency distribution of the human cochlea with varying CDL shows substantial interindividual differences. The aim of this work is to provide an overview of the methods used to determine the cochlear parameters as well as of relevant studies on the CDL, the number and distribution of SGZ, and the frequency assignment of electrode contacts. Based on this, aconcept for individualized cochlear implantation will be presented. In summary, this work should help to promote individualized medicine in the field of cochlear implants in the future, in order to overcome current limitations and optimize audiological outcomes.

Quantitative assessment of cochlear and vestibular ganglion neurons in temporal bones with chronic otitis media.

In this study, we aimed to determine whether or not COM leads to loss of spiral and Scarpa ganglion neurons. From the human temporal bone (HTB) collection at the University of Minnesota we selected human temporal bones with COM, defined as the presence of clinically intractable tissue abnormalities in the middle ear (cholesteatoma, perforation of the eardrum, granulation tissue, fibrosis, tympanosclerosis, and cholesterol granuloma). We also selected HTBs from donors with no ear diseases as controls. We quantitatively analyzed the number of spiral and Scarpa ganglion cells and compared the results obtained in the control and study groups. In both COM and control groups we observed a significant negative correlation between age and number of both spiral (R = -0.632; P < 0.001; 95% CI - 0.766 to - 0.434) and Scarpa ganglion (R = - 0.404; P = 0.008; 95% CI - 0.636 to - 0.051) cells. We did not find any significant differences in the number of spiral ganglion cells (in total or per segment) or in the density of Scarpa ganglion cells (in each vestibular nerve or both) in the COM group as compared with controls (P > 0.05). Our results did not demonstrate significant loss of cochlear or vestibular peripheral ganglion neuron loss in HTBs with COM as compared with controls.

Tauroursodeoxycholic acid attenuates cisplatin-induced hearing loss in rats

Tauroursodeoxycholic acid (TUDCA) has been reported to be protective against apoptosis and oxidative stress in various cell types. A few studies have demonstrated otoprotective effects of TUDCA in mouse models. This study investigated the otoprotective effects of TUDCA in cisplatin (CXP)-induced hearing-loss rats. Eight-week-old female Sprague-Dawley rats were used. The CXP group received intraperitoneal injection of CXP at a dose of 5 mg/kg from day 1 to day 3. The CXP + TUDCA group received an intraperitoneal injection of 5 mg/kg CXP and 100 mg/kg TUDCA from day 1 to day 3. The mRNA expression levels of heme oxygenase 1 (HO1) and superoxide dismutase 2 (SOD2) were measured, and the protein levels of caspase 3, cleaved caspase 3, and aryl hydrocarbon receptor (AhR) were evaluated. The CXP group demonstrated higher mean auditory brainstem responses (ABR) thresholds than the control group. The mean ABR threshold shifts were lower in the CXP + TUDCA group than in the CXP group. The CXP group showed elevated HO1 and SOD2 mRNA expression levels compared to the control group, but these changes were reversed in the CXP + TUDCA group. Compared to the levels in the control group, caspase 3, cleaved caspase 3, and AhR levels were higher in the CXP group, but the increase in cleaved caspase-3 was attenuated in the CXP + TUDCA group. The cochlea showed a higher number of spiral ganglion cells and outer hair cells in the CXP + TUDCA group than in the CXP group. TUDCA reduced CXP-induced hearing loss in adult rats. The HO1-mediated antioxidative effects attenuated apoptosis in the cochlea, but AhR activation was not reversed.

Spiral ganglion cell degeneration-induced deafness as a consequence of reduced GATA factor activity.

Zinc-finger transcription factors GATA2 and GATA3 are both expressed in the developing inner ear, although their overlapping versus distinct activities in adult definitive inner ear are not well understood. We show here that GATA2 and GATA3 are co-expressed in cochlear spiral ganglion cells and redundantly function in the maintenance of spiral ganglion cells and auditory neural circuitry. Notably, Gata2 and Gata3 compound heterozygous mutant mice had a diminished number of spiral ganglion cells due to enhanced apoptosis, which resulted in progressive hearing loss. The decrease in spiral ganglion cellularity was associated with lowered expression of neurotrophin receptor TrkC that is an essential factor for spiral ganglion cell survival. We further show that Gata2 null mutants that additionally bear a Gata2 YAC (yeast artificial chromosome) that counteracts the lethal hematopoietic deficiency due to complete Gata2 loss nonetheless failed to complement the deficiency in neonatal spiral ganglion neurons. Furthermore, cochlea-specific Gata2 deletion mice also had fewer spiral ganglion cells and resultant hearing impairment. These results show that GATA2 and GATA3 redundantly function to maintain spiral ganglion cells and hearing. We propose possible mechanisms underlying hearing loss in human GATA2- or GATA3-related genetic disorders.

Downregulated UCHL1 Accelerates Gentamicin-Induced Auditory Cell Death via Autophagy.

The clinical use of aminoglycoside antibiotics is partly limited by their ototoxicity. The pathogenesis of aminoglycoside-induced ototoxicity still remains unknown. Here, RNA-sequencing was conducted to identify differentially expressed genes in rat cochlear organotypic cultures treated with gentamicin (GM), and 232 and 43 genes were commonly up- and downregulated, respectively, at day 1 and 2 after exposure. Ubiquitin carboxyl-terminal hydrolase isozyme L1 (Uchl1) was one of the downregulated genes whose expression was prominent in spiral ganglion cells (SGCs), lateral walls, as well as efferent nerve terminal and nerve fibers. We further investigated if a deficit of Uchl1 in organotypic cochlea and the House Ear Institute-Organ of Corti 1 (HEI-OC1) cells accelerates ototoxicity. We found that a deficit in Uchl1 accelerated GM-induced ototoxicity by showing a decreased number of SGCs and nerve fibers in organotypic cochlear cultures and HEI-OC1 cells. Furthermore, Uchl1-depleted HEI-OC1 cells revealed an increased number of autophagosomes accompanied by decreased lysosomal fusion. These data indicate that the downregulation of Uchl1 following GM treatment is deleterious to auditory cell survival, which results from the impaired autophagic flux. Our results provide evidence that UCHL1-dependent autophagic flux may have a potential as an otoprotective target for the treatment of GM-induced auditory cell death.

Endoplasmic reticulum stress is involved in spiral ganglion neuron apoptosis following chronic kanamycin-induced deafness.

Aminoglycoside antibiotics-induced hearing loss is a common sensorineural impairment. Spiral ganglion neurons (SGNs) are first-order neurons of the auditory pathway and are critical for the maintenance of normal hearing. In the present study, we investigated the time-course of morphological changes and the degeneration process of spiral ganglion cells (SGCs) following chronic kanamycin-induced deafness and determined whether the endoplasmic reticulum (ER) stress was involved in the degeneration of SGNs. We detected density changes in SGCs and the expressions of Bip, inositol requirement 1 (IRE1)α, activating transcription factor-6α, p-PERK, p-eIF2α, CHOP, and caspase-12 at each time point after kanamycin treatment. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining was also performed. The number of SGC deletions reached ∼50% at the 70th day after kanamycin administration and the ER of most SGCs were dilated. The expression of p-PERK, p-eIF2α, p-IRE1α, Bip, caspase-12, and Chop was significantly unregulated after kanamycin treatment. The number of SGCs that were positive for both TUNEL and caspase-12 increased from day 7 to 28. Taken together, these data demonstrate that ER stress was involved in kanamycin-induced apoptosis of SGNs. Kanamycin-induced SGN apoptosis is mediated, at least in part, by ER stress-induced upregulation of CHOP and caspase-12.

Photobiomodulation by laser therapy rescued auditory neuropathy induced by ouabain

Auditory neuropathy is a hearing disorder caused by impaired auditory nerve function. The lack of information about the pathophysiology of this disease limits early diagnosis and further treatment. Laser therapy is a novel approach to enhance nerve growth or induce axonal regeneration. We induced auditory neural degeneration sparing the sensory epithelium with local ouabain application in an animal model and observed the rescue effect of photobiomodulation (PBM), showing recovered auditory function and favorable histologic outcome. Hearing was evaluated using the auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE). Seven days after ouabain application, the animals were sacrificed to evaluate the morphological changes. DPOAE change was not observed in all groups after ouabain application indicating no changes of outer hair cell function. Ouabain application increased the ABR thresholds increase, while the use of ouabain plus laser produced lower threshold compared to the ouabain group. Hematoxylin and Eosin staining of cochlea mid-modiolar sections in animals treated with ouabain showed damaged spiral ganglion cells, neurofilaments, and post synaptic puncta. Ouabain plus laser group showed higher number of spiral ganglion cells, higher density of neurofilaments, and higher number post synaptic puncta counts compared with ouabain application group. Short-term application of ouabain caused spiral ganglion cell damage while sparing the inner and outer hair cells in gerbils. Photobiomodulation alleviated the hearing loss caused by ouabain induced auditory neuropathy. The results indicate the possible role of photobiomodulation therapy for inner ear diseases accompanied by spiral ganglion degeneration.

Effects of Intralabyrinthine Hemorrhage on the Cochlear Elements: A Human Temporal Bone Study.

To compare histopathologic findings in the cochlea of human temporal bones with versus without intralabyrinthine hemorrhage. Hemorrhagic labyrinthitis can cause sensorineural damage, sudden hearing loss, and vertigo. Yet, to our knowledge, no studies have quantitatively described histopathologic effects of intralabyrinthine hemorrhage on the elements of the cochlea. We analyzed 46 human temporal bone samples from 23 patients with unilateral intralabyrinthine hemorrhage (23 samples from ears with intralabyrinthine hemorrhage and 23 samples from contralateral ears without). We noted the location of hemorrhage in the inner ear, the degree of endolymphatic hydrops, the number of spiral ganglion cells and hair cells, mean loss of fibrocytes in spiral ligament, and areas of the stria vascularis and spiral ligament. Intralabyrinthine hemorrhage caused significant loss of outer hair cells in the lower basal (p = 0.001), upper basal (p = 0.005), and lower middle (p = 0.012) cochlear turns. The degree of endolymphatic hydrops was significantly different between the hemorrhagic and contralateral sides (p = 0.011). But we found no significant difference between the 2 sides in the number of inner hair cells, spiral ganglion cells, and fibrocytes, or in the areas of the stria vascularis and spiral ligament between the two groups (p > 0.05). These findings suggest that such patients could be good candidates for hearing aid or cochlear implant if they have profound sensorineural hearing loss.

Age-related expression of plasma membrane Ca(2+) -ATPase isoform 2 in the cochleas of C57BL/6J mice

To investigate the location and distribution of plasma membrane Ca²⁺ -ATPase isoform 2(PMCA2) in the cochleas of C57BL/6J mice at various ages (4w, 14w, 22w, 45w), and to reveal the relationship of PMCA2 and age-related hearing loss (AHL). The distribution of PMCA2 in the cochleas of C57BL/6J mice was detected by immunohistochemistry at various ages (4w, 14w, 22w, 45w). Real-time polymerase chain reaction (Rt-PCR) was used to detect the level of PMCA2 mRNA in the cochleas of C57BL/6J mice at the ages of 4, 14, 22 and 45 weeks old respectively. Using SPSS17.0 software for statistical analysis. PMCA2 was mainly located in the hear cells, stria vascularis, and spiral ganglion cells. Faint labeling of PMCA2 was also observed in spiral ligament. Hair cells missed and the number of spiral ganglion cells reduced with age. Expression of PMCA2 in the cochleas of C57BL/6J mice also showed age-related decreasing. The results of Rt-PCR demonstrated the expression of mRNA of gene (Atp2b2) at 14 weeks age was significantly less than 4 week-old mice cochlears (P<0.05). The expression of mRNA of gene (Atp2b2) at 22 weeks age was significantly less than 14 week-old mice cochlears (P<0.05). The expression of mRNA of gene (Atp2b2) at 45 weeks age was significantly less than 14 week-old mice cochlears (P<0.01). PMCA2 is mainly located in the hear cells, stria vascularis, and spiral ganglion cells. Faint labeling of PMCA2 is also observed in spiral ligament. The expression of PMCA2 demonstrates an age-related decrease with age. The mRNA expression level of PMCA2 gene(Atp2b2) in the cochleas of C57BL/6J mice displayed an age-related decrease. PMCA2 transporters may play a critical role in maintaining the normal morphology of the inner ear and it may be related to AHL.

Cochlear changes in serous labyrinthitis associated with silent otitis media: A human temporal bone study

PurposeTo determine histopathological findings in the cochlea of human temporal bones with serous labyrinthitis. Materials and methodsWe compared human temporal bones with serous labyrinthitis (20 cases) associated with silent otitis media and without serous labyrinthitis (20 cases) to study location of serous labyrinthitis, the degree of endolymphatic hydrops, number of spiral ganglion cells and hair cells, loss of fibrocytes in the spiral ligament, and areas of the spiral ligament and stria vascularis. ResultsThe serous labyrinthitis caused significant loss of outer hair cells in the lower basal (P=0.006), upper basal (P=0.005), and lower middle (P=0.011) cochlear turns, and significant increase in the degree of endolymphatic hydrops than the control group (P=0.036). No significant difference was found in the loss of inner hair cells, in the number of spiral ganglion cells and fibrocytes in the spiral ligament, and in areas of the stria vascularis and spiral ligament (P>0.05). ConclusionsSerous labyrinthitis resulted in significant loss of outer hair cells and significant increase in the degree of endolymphatic hydrops.

Neurogenesis of the spiral ganglion cells in the cochlea requires the transcriptional cofactor TIS21

The molecular mechanisms controlling the proliferation and differentiation of spiral ganglion cells (SGCs) in the inner ear are still largely unknown. TIS21 is a transcriptional cofactor that shows antiproliferative, antiapoptotic, and prodifferentiative effects on neural progenitor cells. To investigate the function of TIS21 during SGC development, we analyzed SGC neurogenesis from embryonic day 13.5 (E13.5) to postnatal day 4 (P4) in Tis21-GFP knock-in mice, in which the protein-encoding exon of the Tis21 gene was replaced by EGFP. Through E13.5 to P4, we found fewer SGCs in homozygous Tis21-GFP knock-in mice than in wild-type mice. Our results suggest that TIS21 is required for development of SGCs. Deleting Tis21 may affect progenitor cells or neuroblasts at the beginning of cochlear-vestibular ganglion formation and would consequently lead to a decrease in the number of SGCs.

Role of macrophage migration inhibitory factor in age-related hearing loss

Hearing loss related to aging is the most common sensory disorder among elderly individuals. Macrophage migration inhibitory factor (MIF) is a multi-functional molecule. The aim of this study was to identify the role of MIF in the inner ear. MIF-deficient mice (MIF−/− mice) of BALB/c background and wild-type BALB/c mice were used in this study. Expression of MIF protein in the inner ear was examined by immunohistochemistry in wild-type mice (WT). The hearing function was assessed by the click-evoked auditory brainstem response in both MIF−/− mice and WT at 1, 3, 6, 9, 12, and 18months of age. Morphological examination of the cochlea was also performed using scanning electron microscopy and light microscopy. MIF was observed in the spiral ligament, stria vascularis, Reissner’s membrane, spiral ganglion cells (SGCs), saccular macula, and membranous labyrinth. The MIF−/− mice had a significant hearing loss as compared with the WT at 9, 12, and 18months of age. In the MIF−/− mice, scanning electron microscopy showed that the outer cochlear hair cells were affected, but that the inner cochlear hair cells were relatively well preserved. The number of SGCs was lower in the MIF−/− mice. MIF was strongly expressed in the mouse inner ear. Older MIF−/− mice showed accelerated age-related hearing loss and morphological inner ear abnormalities. These findings suggest that MIF plays an important role in the inner ear of mice.

Exogenous IL-4-expressing bone marrow mesenchymal stem cells for the treatment of autoimmune sensorineural hearing loss in a guinea pig model.

Bone marrow mesenchymal stem cells (BMSCs) expressing recombinant IL-4 have the potential to remediate inflammatory diseases. We thus investigated whether BMSCs expressing exogenous IL-4 could alleviate autoimmune sensorineural hearing loss. BMSCs isolated from guinea pigs were transfected with recombinant lentivirus expressing IL-4. A total of 33 animals were divided into three groups. Group A received scala tympani injection of IL-4-expressing BMSCs, and Group B received control vector-expressing BMSCs, and Group C received phosphate-buffered saline. The distribution of implanted BMSCs in the inner ears was assessed by immunohistochemistry and fluorescence microscopy. Auditory brain-stem response (ABR) was monitored to evaluate the auditory changes. Following BMSCs transplantation, the threshold levels of ABR wave III decreased in Groups A and B and significant differences were observed between these two groups (P < 0.05). Transplanted BMSCs distributed in the scala tympani and scala vestibuli. In some ears with hearing loss, there was a decrease in the number of spiral ganglion cells and varying degrees of endolymphatic hydrops or floccule. Following transplantation, the lentivirus-infected BMSCs migrated to the inner ear and produced IL-4. Our results demonstrate that, upon transplantation, BMSCs and BMSCs expressing recombinant IL-4 have the ability to remediate the inflammatory injury in autoimmune inner ear diseases.

Spiral ganglion cell morphology in guinea pigs after deafening and neurotrophic treatment

It is well known that spiral ganglion cells (SGCs) degenerate in hair-cell-depleted cochleas and that treatment with exogenous neurotrophins can prevent this degeneration. Several studies reported that, in addition, SGC size decreases after deafening and increases after neurotrophic treatment. The dynamics of these cell size changes are not well known. In a first experiment we measured size, shape (circularity) and intracellular density of SGCs in guinea pigs at various moments after deafening (1, 2, 4, 6, and 8 weeks) and at various cochlear locations. In a second experiment, the effect of treatment with brain-derived neurotrophic factor (BDNF) on SGC morphology was investigated at various cochlear locations in deafened guinea pigs. We found that SGC size gradually decreased after deafening in the basal and middle cochlear turns. Already after one week a decrease in size was observed, which was well before the number of SGCs started to decrease. After BDNF treatment SGCs became noticeably larger than normal throughout the cochlea, including the middle and apical turns, whereas an effect on survival of SGCs was primarily observed in the basal turn. Thus, both after deafening and after neurotrophic treatment a change in size occurs before survival is affected. Morphological changes were not restricted to a subpopulation of SGCs. We argue that although changes in cell size and changes in survival might be manifestations of two separate mechanisms, morphological measures such as size, circularity and intracellular density are indicative for survival and degeneration.

Inner Ear Changes in Mucopolysaccharidosis Type I/Hurler Syndrome

Mucopolysaccharidosis type I/Hurler syndrome is an autosomal recessive disease caused by a deficiency of α-L-iduronidase activity. Recurrent middle ear infections and hearing loss are common complications in Hurler syndrome. Although sensorineural and conductive components occur, the mechanism of sensorineural hearing loss has not been determined. The purpose of this study is to evaluate the quantitative inner ear histopathology of the temporal bones of patients with Hurler syndrome. Eleven temporal bones from 6 patients with Hurler syndrome were examined. Age-matched healthy control samples consisted of 14 temporal bones from 7 cases. Temporal bones were serially sectioned in the horizontal plane and stained with hematoxylin and eosin. The number of spiral ganglion cells, loss of cochlear hair cells, area of stria vascularis, and cell density of spiral ligament were evaluated using light microscopy. There was no significant difference between Hurler syndrome and healthy controls in the number of spiral ganglion cells, area of stria vascularis, or cell density of spiral ligament. The number of cochlear hair cells in Hurler syndrome was significantly decreased compared with healthy controls. Auditory pathophysiology in the central nerve system in Hurler syndrome remains unknown; however, decreased cochlear hair cells may be one of the important factors for the sensorineural component of hearing loss.

Minimally Invasive Drug Delivery to The Cochlea Through Application of Nanoparticles to The Round Window Membrane

Direct drug delivery to the cochlea is associated with the risk of irreversible damage to the ear. In this study, liposome and polymersome nanoparticles (NPs), both formed from amphiphilic molecules (lipids in liposomes and block copolymers in polymersomes), were tested as potential tools for drug delivery to the cochlea via application onto the round window membrane in adult mice (strain C3H). One day after round window membrane application, both types of NPs labeled with fluorescent markers were identified in the spiral ganglion in all cochlear turns without producing any distinct morphological or functional damage to the inner ear. NPs were detected, although to a lesser extent, in the organ of Corti and the lateral wall. The potential of liposome and polymersome NPs as therapeutic delivery systems into the cochlea via the round window membrane was evaluated using disulfiram, a neurotoxic agent, as a model payload. Disulfiram-loaded NP delivery resulted in a significant decrease in the number of spiral ganglion cells starting 2 days postapplication, with associated pronounced hearing loss reaching 20-35 dB 2 weeks postapplication as assessed through auditory brainstem responses. No changes in hair cell morphology and function (as assessed by recording otoacoustic emissions) were detected after disulfiram-loaded NP application. No effects were observed in controls where solution of free disulfiram was similarly administered. The results demonstrate that liposome and polymersome NPs are capable of carrying a payload into the inner ear that elicits a biological effect, with consequences measurable by a functional readout.

From High-Tech to Biotech Using Stem Cell and Gene Therapy to Treat Hearing Loss

From High-Tech to Biotech Using Stem Cell and Gene Therapy to Treat Hearing Loss

Cochlear Otosclerosis Adjacent to Round Window and Oval Window

The purpose of this histopathological study is to examine temporal bones of patients with cochlear otosclerosis adjacent to the round window or adjacent to the oval window as compared with healthy controls. It is unclear if the extent and site of otosclerosis affects the extent of damage to cochlear structures and hearing loss. Twelve temporal bones from 10 patients with cochlear otosclerosis adjacent to the round window, 11 temporal bones from 8 patients with cochlear otosclerosis adjacent to the oval window, and 12 bones of healthy age-matched controls were selected for study. We calculated the number of spiral ganglion cells, changes in cochlear structures, the extent and site of cochlear otosclerosis, and audiometric data. The loss of spiral ganglion cells and the absence of outer hair cells in patients with cochlear otosclerosis adjacent to the round window were significantly higher than those in patients with cochlear otosclerosis adjacent to the oval window and healthy controls. The area of the spiral ligament in patients with cochlear otosclerosis adjacent to the oval window was significantly smaller than that in healthy controls. However, no significant difference was found in the spiral ligament of patients with cochlear otosclerosis adjacent to the round window and healthy controls. There was no significant difference between patients with cochlear otosclerosis and age-matched controls in audiometric data. Cochlear otosclerosis adjacent to the round window caused significantly more damage to spiral ganglion cells and outer hair cells than cochlear otosclerosis adjacent to the oval window without loss of spiral ligament.

Cochlear changes in presbycusis with tinnitus

Objectives The pathophysiology of tinnitus is obscure and its treatment is therefore elusive. Significant progress in this field can only be achieved by determining the mechanisms of tinnitus generation, and thus, histopathologic findings of the cochlea in presbycusis with tinnitus become crucial. We revealed the histopathologic findings of the cochlea in subjects with presbycusis and tinnitus. Material and methods The subjects were divided into 2 groups, presbycusis with tinnitus (tinnitus) group and presbycusis without tinnitus (control) group, with each group comprising 8 temporal bones from 8 subjects. We quantitatively analyzed the number of spiral ganglion cells, loss of cochlear inner and outer hair cells, and areas of the stria vascularis and spiral ligament. Results There was a significantly greater loss of outer hair cells in the tinnitus group compared with the control group in the basal and upper middle turns. The stria vascularis was more atrophic in the tinnitus group compared with the control group in the basal turn. Conclusions Tinnitus is more common in patients with presbycusis who have more severe degeneration of outer hair cells and stria vascularis.