[Deviations of the head in the Romberg position and deviations in the vestibular reaction to sound in essential vascular disorders of the labyrinth].
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Ten deaf-mute subjects with total vestibular areflexia were subjected to positional tests, i.e. assessment of the postural subjective vertical and horizontal plane by deviations in the frontal and sagittal plane. The tests were performed in the author's modification of a Grahe table. Comparison with the results of 10 healthy subjects revealed that extinction of vestibular activity increases the inaccuracy of assessment of the body position in space. The conclusion is: the vestibular (otolith) apparatus supplements and makes the activity of all other gravireceptors more accurate but not hold a dominant place among them.
The symptom of sudden tilting of the visual surroundings is described in detail based on experience with five patients. Patients perceive the visual fields as suddenly turning through a variable arc, most frequently 90-180 degrees, usually associated with dizziness. In three patients with vertebral-basilar artery disease, visual tilting was more closely related to local pontomedullary ischemia than to posterior cortical ischemia. It is suggested that most instances of this illusion are due to disorders of the vestibular-otolithic apparatus or its central connections, most frequently from vertebral-basilar ischemia.
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In the frog immobilized by intralymphatic injection of D-tubocurarine, stimulation of the visual apparatus with either electrical shocks applied to the optic chiasma or light pulses elicited, in many cases, an increase and a decrease of firing of efferent and afferent vestibular neurons, respectively, recorded from the horizontal semicircular canal nerve. Optokinetic stimulation was completely inefficient in modulating the efferent and afferent discharge. These results show that stimulation of the visual system can modify vestibular apparatus fuctioning at the most peripheral level. However, it is likely that the effects observed were due to an arousal phenomenon or/and to a motor corollary discharge.
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In vertebrates, the paired-box transcription factor Pax-2 is one of the earliest markers of the developing inner ear and is robustly expressed in the otic placode and the otic vesicle. Mutations in the Pax-2 gene result in developmental defects of the vestibular and auditory apparatus. We set out to investigate whether regions of Pax-2 expression in the developing otic vesicle correlate with areas of cell proliferation or cell death, which would indicate a possible role of Pax-2 in these processes. Regionalized proliferation and local apoptosis are the principal mechanisms that lead to the complex morphogenesis of the highly compartmentalized inner ear starting from a simple vesicle. We found a high correlation of Pax-2 expression with proliferating cells in the walls of the early otic vesicle. Apoptotic cells were mostly localized outside of the Pax-2-expressing regions. At later stages, we found the highest intensity of proliferating and Pax-2-positive cells in areas of the developing sensory epithelia. When hair cells begin to differentiate, they maintain a lower level of Pax-2 expression than neighboring cells for a brief period, before they completely down-regulate expression of this transcription factor. We conclude that a significant proportion of proliferating cells in the developing otocyst express Pax-2, in particular in regions that include developing sensory patches. This implicates Pax-2 as a marker for proliferating hair and supporting cell progenitors. Furthermore, the likelihood that Pax-2-expressing cells in the otocyst die by apoptosis is much lower when compared with cells residing in Pax-2-negative regions.
After orbital space flights lasting 19.5--22.5 days, disturbances are observed in mineral metabolism in rats, which are morphologically manifested as osteoporosis of the spongy sections of long hollow skeletal bones, periosteocytic osteolysis of them, atrophy and dystrophy of skeletal muscles, and inhibition of erythroid growth of bone marrow, which occurred and developed in weightlessness as a result of deprivation of motor activity due to removal (or reduction) of static load from the musculoskeletal system. Development of stress reaction, which is apparently intensified at certain stages of flight (lift off and touchdown) and during transition from weightlessness to conditions of gravitational force on earth, leads to corresponding changes in the structure and cellular composition of lymphoid organs, and to changes in the hypothalamic-hypophyseal neurosecretory system, adrenal glands, and other organs. Changes in the receptor apparatus of the vestibular system are associated with local circulatory changes occurring during weightlessness and G forces, while retinal injuries are associated with the effect of heavy charged particles of cosmic radiation. All changes are reversible and disappear completely or to a substantial degree a month after completion of the flight.
There are several mechanisms whereby alteration of barometric pressure can produce vertigo in divers or aviators. Development of a reliable measure of vestibular function in an animal model is the first requirement for further study of these mechanisms. This report presents the development of a rotatory table device capable of evoking the vestibulo-ocular reflex (VOR) of a guinea pig while in a hyperbaric chamber. To assess the reproducibility of this response, eight animals were monitored by electronystagmography during rotations at three table velocities (62.4, 83.3, and 100 degrees/s). Two test sessions were performed on each animal with a 6-hour interval between sessions. The VOR gain was calculated by dividing the average peak velocity of the slow phase component of the nystagmus by the peak stimulus velocity. At least eight observations per test speed were averaged; calibration of eye movement was performed prior to each session by forced ocular abduction. Multifactorial analysis of variance revealed no significant differences (p > .05) between the differing rotation speeds nor between test sessions for individual animals. However, there was a significant difference in VOR gain between animals (p < .002). The VOR gain was then measured, using the same techniques, in another group of seven animals before, during, and after an air dive to the equivalent of 200 feet of seawater (7.06 atmospheres absolute) to assess the effects of nitrogen narcosis. Pre- and post-dive VOR gains were significantly greater than those measured at depth (p < .05). These results are consistent with the slow processing model of nitrogen narcosis and the controversial theory that central nervous system depressants decrease the VOR gain. The results also demonstrate the ability of this inexpensive apparatus to provide a sensitive measure of pressure-induced changes of vestibular function in guinea pigs.