In order to advance our scientific endeavors in the field of vestibular-spatial orientation research, it is important to know how much research has already been carried out, and how much accurate information we currently possess. It is mandatory to have sufficient background information in order to establish a solid working hypothesis utilizing insightful approaches. Accordingly, this historical survey covers various research endeavors from the beginning of aviation until the end of 2001, including Skylab, Microgravity Vestibular Investigations, and Neurolab.
Integration mechanisms of multisensory modality in the brain are described in relation to formation of spatial orientation. Vestibular, visual and somatosensory (proprioceotive) informations are essential component in forming spatial orientation and spatial memory. The parietal association cortex is the most plausible location to convert multisensory informations into spatial orientation, while the hippocampus is one of the places to store and retrieve the built-up spatial memory (spatial orientation). Then a new hypothesis was proposed to explain the gensis of SAS (space adaptation syndromes), by considering spatial disorientation and other sensory conflicts.
A new care system has been established, although the majority of the otorhinolaryngologists have not yet taken part in this new care system. Based on the results of a questionnaire sent to active members of the Japan Society for Equilibrium Research, 22 patients with dizziness and disequilibrium were judged to need care. We report the characteristics of the activities of daily living of these patients. Based on our experience, evaluating the activities of daily living is useful in describing opinions regarding care.
Positional nystagmus and positional vertigo are usually successfully cured by Epley's repositioning maneuver in BPPV, but most of the patients still complain dizzy sensation after the treatment. In this paper, body equilibrium function while standing was investigated by stabilometry with eyes closed in 11 cases of BPPV before and after treatment with repositioning maneuver. These subjects were followed for 4 weeks. In all patients, 75 mg/day of difenidol hydrochloride and 300 mg/day of ATP was medicated. Five of 11 these patients still complained of dizziness or floating sensation 4 weeks after the repositioning maneuver. The total length and the area of the center of gravity was above the standard levels in 6 and 7 of 11, respectively, before the repositioning maneuver. Four of 11 in both total length and area showed abnormalities 4 weeks after treatment with the repositioning maneuver. Between the value of the total length, area and ratio of total length by area before and 4 weeks after treatment did not change, which was statistically confirmed by t-test. Canal dysfunction in canalolithasis of posterior semicircular canal was improved by repositioning maneuver, however, dizzy sensation and unsteadiness during standing with eyes shut, which are supposed to be due to otolith dysfunction, was not influenced by the treatment. Medication and vestibular rehabilitation should be considered to treat persistent dizziness and body dysequilibrium after Epley's maneuver in BPPV.
Visually induced self-motion (vection) is of theoretical interest in understanding the neural basis of visual-vestibular interaction. Recently, vection is also of practical importance in developing virtual reality systems that provide users with a compelling experience of "presence" in a virtual environment. The purpose of this paper was to investigate the role of the central and peripheral retina in visually induced self-rotation (circular vection, CV). Six patients aged 52-78 years all with pathological peripheral visual defects due to retinitis pigmentosa or glaucoma, and an age-matched control group of eight elderly subjects aged 47-71 years were examined. Monocular visual field defects were verified with the Goldmann perimeter by kinetic perimetry. The device used to induce CV was a random dot pattern projected onto a hemispherical dome with a radius of 75 cm. The pattern was rotated horizontally at a constant acceleration of 1 deg/s2. Monocular stimuli were randomly repeated twice in both the temporal-nasal (T-N) and nasal-temporal (N-T) directions. In the age-matched control group, all subjects experienced CV. There were no significant differences in CV latencies between the right and left eyes in either stimulus direction (p>0.05, Student paired t test). In patients with bilateral deficits of the whole visual periphery and intact central visual fields, CV was absent in both stimulus directions. In patients with bilateral and asymmetric deficits of the visual periphery, CV was either missing or markedly prolonged, depend-ing on the extent of the peripheral visual field defect. In patients with unilateral deficits of about half the visual periphery, CV was missing only for the affected eyes. These findings are compatible with the theory of peripheral dominance and size dependence of CV. In the discussion, our results will be compared to previous experiments with masking in normal subjects and with studies in other kinds of self-motion.
Peripheral positional vertigo is the most common type of vertigo due to peripheral vestibular lesion. Recently, peripheral positional vertigo is classified according to different lesions of originating in the canal. The posterior canal positional vertigo is so called benign paroxysmal positional vertigo. In horizontal canal positional vertigo of cupulolithiasis, the direction-changing horizontal ageotropic nystagmus is caused by cupulolithiasis, these patients cannot be diagnosed early. In addition, the attack period tends to persist for a few months. Therefore, we developed a new method of a head-shaking in anteflexio while sitting. In this study, two patients with horizontal canal positional vertigo of cupulolithiasis performed anteflexio head-shaking while sitting and were examined using an infrared CCD camera. By anteflexio head-shaking while sitting, we were able to easily transfer horizontal canal positional vertigo of cupulolithiasis to canalolithiasis. Furthermore, positional nystagmus disappeared by the modified Lempert method.