The melanocytes of the vestibular labyrinth as seen in colored guinea pigs show a characteristic pattern of distribution in the wall of the utricle and in the ampullae, but they are not present in the wall of the saccule. They are found mainly in well-vascularized regions of apparent secretory or metabolic importance, including the "dark cell" areas. Their dendrite-like processes are often in intimate contact with the capillaries, although no pinocytotic vesicles or other indications of transfer of substances between the melanocytes and the capillary endothelium are seen under the electron microscope. In the human ear, the apparent density of the melanocytes varies with skin color. They are numerous in the cochlea, especially in the bony wall of the modiolus and on the osseous spiral lamina, and they occur also in Reissner's membrane and in the stria vascularis. In the vestibular system they are found in the wall of the saccule as well as in the utricle, the crus commune, and the ampullae, but not in the semicircular canals. They tend to be diffusely scattered, rather than to fonn the well-defined, intensely pigmented areas that are characteristic of the guinea pig. Close contacts with capillaries are seen mainly in the tympanic portion of the spiral ligament. The significance of melanin and the melanocytes in the labyrinth is unknown, but both the anatomical relation of certain melanocytes to capillaries, and the biocheInical relation of melanin to the catecholamines support the hypothesis that they may have a vasomotor function. Other evidence, including the not infrequent association of sensorineural deafness with hereditary disorders of pigmentation also suggests that the melanocytes may play a role of some biological consequence in the inner ear.
Patients with perilymphatic fistula have been described as having symptoms similar to Meniere's disease and endolymphatic hydrops. Direct clinical or experimental evidence linking the two inner ear disorders has been lacking. An enhancement of the summating potential observed with electrocochleography suggests a diagnosis of ELH in both of these inner ear disorders. In this study, ECoG results of 27 patients with surgically confirmed PLF are reported. Fourteen patients with surgically confirmed spontaneous PLF had abnormal ECoG. Six of these 14 patients had normal hearing. The ECoG changes in patients with Meniere's disease and those with surgically confirmed PLF are identical, indicating the underlying pathologic change in both is hydrops. But there is no specific diagnostic abnormality on ECoG that differentiates these two inner ear disorders. Also, an experimental model of PLF was developed and studied in guinea pigs. "Inactive" PLF is defined as "an opening was made into the cochlea, but if no perilymph moved out through the fistula, it was defined as inactive" An "active" PLF occurs when perilymph actually moves from the inner ear out to the middle ear. ECoGs were recorded before and after creation of an "active" PLF. ECoG abnormalities were seen in "active" PLF and correlated with histologic data demonstrating ELH. An abnormally enhanced summating potential was demonstrated after active removal of perilymph through the experimentally created fistula. Cochlear duct histology showed hydropic distention of Reissner's membrane in the experimental ears and no changes in the membranous labyrinths of the unoperated, control ears.(ABSTRACT TRUNCATED AT 250 WORDS)
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