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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Scanning electron microscopy and immunoglobulins of the endolymphatic sac in normal human subjects and sensorineural deafness. With special reference to Menière's disease.

The pathophysiology of the endolymphatic sac (ES) in Meniere's disease was studied by scanning electron microscopy and staining of immunoglobulins in the intradural portion of the ES. The peroxidase-antiperoxidase method by means of paraffin sections was used for staining of immunoglobulins. First, subjects without hearing impairment and malformation of the temporal bone, ranging from a 7-month-old fetus to an 80-year-old adult, were investigated. All subjects, including fetuses, showed well-arranged epithelial cells by scanning electron microscopy. The epithelial cells in the proximal portion of the intradural ES were oval, showing a tendency of transitional change to be flat as they drew near the distal portion of the ES. The epithelial cells consisted mostly of light cells, but sporadic dark cells were seen. Regarding the immunoglobulins. IgG was slightly positive in the epithelial and subepithelial layers. All 15 patients with Meniere's disease showed various types of degeneration of the epithelial cells though to varying degrees. However, these findings were also seen in cases of cochlear deafness. On the other hand, the ES of acoustic tumors, with retrocochlear or neural deafness revealed a normal finding, as found in healthy subjects. Inner ear deafness experimentally produced in animals by Kanamycin sulfate (KM) injection showed degeneration of the epithelial cells of the ES similar to that found in human cochlear deafness. IgG of the ES in Meniere's disease showed moderately evident deposits compared to normal subjects. However, this was also found not only in inner ear deafness other than Meniere's disease, but also in animal deafness experimentally produced by KM injection. It is very interesting to note that moderate endolymphatic hydrops was found in animals one year after Preyer's reflex had disappeared. It is postulated that endolymphatic hydrops develop because of impairment of endolymphatic fluid resorption at the rugose portion and stenosis of the lumen in the same portion, due to degeneration of the epithelial cells. From the above results, it is argued that degenerated epithelial cells and immunoglobulins of the ES in Meniere's disease may arise from the sequelae of cochlear deafness. It is also hypothesized that endolymphatic hydrops--at least in the terminal stage of Meniere's disease--may be consistent with the same pathophysiological conditions as in animal experiments.[1]


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