Publicación Oficial de la Sociedad Ecuatoriana de Neurología, de la Liga Ecuatoriana Contra la Epilepsia y de la Sociedad Iberoamericana de Enfermedad Cerebrovascular

ototoxicidad

 

Pathological changes induced by ototoxicity on spiral ganglion neurons and its peripheral processes.

Deafness is one of the most widespread disabilities in the world. Its most frequent cause is death of cochlear hair cells (located in the organ of Corti), which induces degeneration of spiral ganglion neurons and their peripheral processes innervating the organ of Corti. In a previous light microscopy study using a rat model of ototoxicity, a loss of spiral ganglion neurons was observed since the eighth week of deafness and peripheral processes degeneration since the fourth week. In order to determine the onset of ultrastructural degenerative changes, a transmission electron microscopy study of spiral ganglion neurons and their peripheral processes was undertaken. Rat cochleae sampled after 2, 4, 8 and 16 weeks of deafness and healthy controls were analyzed. Since the fourth week of deafness, Type I spiral ganglion neurons and the myelin sheaths of their peripheral processes showed progressive degenerative changes. Most of the remaining neurons exhibited complete demyelination at sixteen weeks of deafness, resulting in the pathological type III spiral ganglion neurons. These results show ultrastructural degenerative changes of the spiral ganglion neurons and their peripheral processes, before both undergo significant losses.

 

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Morphological Changes Induced by Three Aminoglycosides on the Cochlear Stria Vascularis.

Aminoglycosides are efficient antimicrobials commonly used in clinical practice. Their effects on the cells of the organ of Corti and the spiral ganglion neurons have been extensively studied. However, there are only a few reports concerning aminoglycoside-induced morphological changes on the stria vascularis. The purpose of this study was to describe morphological and morphometrical changes on the rat stria vascularis after a profound sensorineural hearing loss induced by three aminoglycosides (kanamycin, gentamicin and amikacin) followed by furosemide. To analyze the stria vascularis area and the number of blood capillaries per stria vascularis, cochleae from fourteen rats sampled at eight weeks after deafness and from four control animals were processed. Serial semi thin cochlear sections from the apical, upper middle, lower middle and basal turns were examined under a light microscope. The cochlear damage degree depended on the aminoglycoside. Mean stria vascularis areas for both kanamycin and gentamicin groups were lower than controls. The mean number of blood capillaries per stria vascularis was reduced for the three aminoglycoside-deafened groups as compared to control animals. For both variables, the most severe damage was observed for gentamicin-deafened animals, followed by kanamycin and amikacin.

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