Temporal Bone Pathology Secondary to Head Trauma-A Human Temporal Bone Study.

HYPOTHESIS/BACKGROUND: We hypothesize that following head trauma there is a difference in temporal bone (TB) pathology in cases with and without skull fracture. Although conductive, sensorineural, mixed hearing loss, and TB pathology following head trauma have been reported, to our knowledge, there are no studies that have compared the pathology of the TB in cases with and without skull fracture. METHODS: We analyzed 34 TBs from donors who had a history of head trauma (20 with skull fracture and 14 without fracture), and 25 age-matched controls without clinical or histological evidence of otologic disorders. We documented the presence and location of TB fracture, ossicular injury, and cochlear hemorrhage and evaluated the loss of spiral ganglion cells and sensory hair cells, damage to the stria vascularis, and the presence of endolymphatic hydrops. RESULTS: We found a significant loss of outer hair cells in the upper basal, lower, and upper middle turns of the cochlea (p = 0.009, =0.019, =0.040, respectively), a significant loss of spiral ganglion cells (p = 0.023), and cochlear hemorrhage predominantly in the basal turns secondary to head trauma. Interestingly, these findings were significantly observed in TBs from donors with a history of head trauma without skull fracture. CONCLUSION: The greatest damage was to the cochlear basal turn. Our findings suggest that head trauma may result in tonotopic high frequency sensorineural hearing loss. TBs from donors with skull fracture have less pathologic changes than those without.

Histopathology of Inner Ear Malformations: Potential Pitfalls for Cochlear Implantation.

HYPOTHESIS: The presence of bony inner ear malformations may associate with a number of anatomical abnormalities affecting the middle ear structures. Those malformations may create pitfalls and complications for cochlear implantation. BACKGROUND: Inner ear malformations associate with varying degrees of hearing loss, and frequently require cochlear implantation for hearing rehabilitation. Therefore, the abnormalities affecting the middle- and inner-ear structures may increase the risk of surgical complications. METHODS: We examined 38 human temporal bones from donors with bony inner ear malformations. Using light microscopy, we analyzed the presence of abnormalities in the structures of the middle- and inner-ear. RESULTS: Our collection comprises of 38 specimens with inner-ear malformations (cochlear aplasia, n = 3; cochlear hypoplasia, n = 30; incomplete partition, n = 3; isolated vestibular malformation, n = 2). The anatomy of the middle ear was abnormal in most temporal bones with cochlear aplasia, cochlear hypoplasia, and incomplete partition type I (40%-100%). Some of those abnormalities (hypoplastic or obliterated mastoid, 55.2%; aplastic or obliterated round window, 71.0%; aberrant course of the facial nerve, 36.8%) may hinder the access to the round window using the conventional facial recess approach for cochlear implantation. The cochlear nerve and associated bony structures (internal auditory canal and bony canal for cochlear nerve) were normal in 71.0% of all temporal bones with inner ear malformations. CONCLUSION: Each different type of malformation may create specific surgical challenges to surgeons. Comprehensive preoperative imaging is fundamental toward the surgical success of cochlear implants in patients with malformations. Alternatives to circumvent those middle- and inner-ear abnormalities and potential complications are further discussed.

Cochleosaccular (Scheibe) dysplasia in dogs: A temporal bone study.

The objective of this study was to evaluate any otopathologic changes in temporal bone specimens from dogs with deafness related to cochleosaccular (Scheibe) dysplasia (CSD). We used the canine temporal bone collections of the Otopathology Laboratory at the University of Minnesota and of the Massachusetts Eye and Ear Infirmary at Harvard University in Boston. Our morphometric analysis included measuring the areas of the stria vascularis and the spiral ligament and counting the number of spiral ganglion cells. In addition, we noted the presence of the organ of Corti and cochlear hair cells, assessed the location of Reissner's membrane and the saccular membrane, and counted the number of both Type I and Type II vestibular hair cells in the macule of the saccule and vestibular ganglion cells. In the group of specimens from dogs with cochleosaccular dysplasia, we observed generalized degeneration in the cochlea and a significantly decreased number of Type I and Type II vestibular hair cells and vestibular ganglion cells. As hereditary deafness is presently untreatable with known therapeutic methods, dogs with cochleosaccular dysplasia should not be considered for breeding. Future therapeutic approaches, such as stem cell therapies, should be designed to target all the elements of the cochlea in addition to the saccule as it was found that both are affected in dogs with CSD.

L'objectif de la présente étude était d'évaluer tous changements otopathologiques dans des spécimens d'os temporal provenant de chiens avec surdité reliée à de la dysplasie cochléosacculaire (Scheibe) (DCS). Nous avons utilisé la collection d'os temporal canin du Otopathology Laboratory à l'Université du Minnesota et du Massachusetts Eye and Ear Infirmary de l'Université Harvard à Boston. Notre analyse morphométrique incluait de mesurer les régions de la stria vascularis et du ligament spiral et de compter le nombre de cellules du ganglion spiral. De plus, nous avons noté la présence de l'organe de Corti et des cellules ciliées cochléaires, évalué la localisation de la membrane de Reissner et de la membrane sacculaire, et compté le nombre de cellules ciliées vestibulaires de Type I et Type II dans la macule du saccule et les cellules vestibulaires ganglionnaire. Dans le groupe de spécimens provenant de chiens avec dysplasie cochléosacculaire, nous avons observé une dégénérescence généralisée de la cochlée et une diminution significative du nombre de cellules ciliées de Type I et Type II et ces cellules du ganglion vestibulaire. Étant donné que la surdité héréditaire est présentement non-traitable par des méthodes thérapeutiques connues, les chiens avec de la dysplasie cochléosacculaire ne devraient pas être utilisés pour la reproduction. Des approches thérapeutiques futures, telles que les thérapies avec des cellules souches, devraient être planifiées afin de cibler tous les éléments de cochlée en plus du saccule étant donné qu'il a été démontré que les deux sont affectés chez les chiens avec DCS.(Traduit par Docteur Serge Messier).