[Catecholamine excretion in labyrinth disease patients].
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The end-organs of the human vestibular system were studied with transmission electron microscopic and freeze-fracturing techniques. The general morphology of the sensory epithelia was comparable to that of animals. The hair cells consisted of flask-shaped type I hair cells with the surrounding nerve calyx and rod-shaped type II hair cells contacted by several small bouton-shaped nerve endings. The hair cells were coupled to neighboring supporting cells by tight junctions at the lateroapical aspect. These were regular in appearance and of the moderately tight type. This type of tight junction has been found elsewhere in the inner ear and is believed to be competent to maintain its unique ion composition. The lateral surfaces of the supporting cells were coupled by gap junctions. The afferent nerve terminal of the type I hair cell, the so-called calyx, totally encompassed the hair cell. It could not be concluded on the basis of the present material whether the type I hair cell-calyx complex mediates electrical or chemical synaptic contact. The synapses of afferent nerves on type II hair cells, however, displayed typical signs of being chemically mediated. Synaptic bodies, similar to those seen in animals, were associated with the presynaptic membrane inside the hair cell. Membrane specializations comparable to those of animals were also seen in these synapses. Efferent nerve endings and synapses were not readily identified and were thus not discussed in this study.
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Based either on spontaneous or experimental vestibular reactions, diagnostic methods proposed by the authors seem most informative for differential diagnosis of internal ear diseases with simulating conditions. The main thing in the above diagnosis is the vestibular testing unit which provides objective synchronous registration of vestibular-somatic and vascular reactions. The necessity of comparing rotatory nystagmus to postnystagmus, the significance of latent spontaneous nystagmus interpretation are emphasized.
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Evidence of hearing loss in humans with systemic autoimmune disease has suggested the possibility of isolated forms of deafness originated by a autoimmune mechanism. Several authors reject McCabe's (1) proposed clinical description based mainly on response to treatment and have attempted to develop an animal model of autoimmune deafness. A comparative analysis was made of several experimental models of sensorineural hearing loss in guinea pigs developed in our laboratory for the study of this problem.
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