Dark cells are found on either side of the vestibular organs. The dark cell epithelium consists of cells with multiple pinocytotic vesicles close to their luminal surface. A large number of infoldings occur at the basal end of the dark cell toward the basal membrane. These infoldings contain numerous mitochondria. The nucleus of the dark cell is displaced toward the surface. Dark cells participate in fluid homeostasis to preserve the unique high-potassium and low-sodium content of the endolymph and also to maintain the calcium homeostasis in the inner ear. The vestibular supporting cells between the sensory cells are in general columnar. Small microvilli are found on the surface and a membrana reticularis is found at the upper surface of the supporting cells. Supporting cells may participate in the generation and the maintenance of the otoconia and the cupula. Supporting cells also participate in the structural support of the sensory cell as well as play an important role in mechanical transduction.
Vertigo is a subtype of dizziness, which can result from lesions in diverse locations such as the inner ear, neck paravertebral stretch receptors, visual and vestibular interaction centers in the brainstem and cerebellum, and in the integrative balance center of the thalamus or cortex. This study focused on vertigo due to various cerebrovascular diseases secondary to vertebrobasilar system diseases including extracranial causes as well as intracranial etiologies. The most common cerebrovascular disorder to cause vertigo, oscillating vision and impulsion was vertebrobasilar insufficiency secondary to atherosclerosis of the subclavian, vertebral and basilar arteries. However, it is not always clear which structures exhibit ischemia. When vertigo is associated with other symptoms of the brainstem, we can assume that vertigo is caused by ischemia in the exact site of the brainstem. Therefore, meticulous clinical neurological examinations are mandatory including bedside neuro-otological examinations before obtaining neuroimaging studies are performed. Knowledge of the mechanisms that underlie vestibular disorders is essential to correctly diagnose and effectively treat patients with vertigo secondary to cerbrovascular diseases.
A 43-year-old women with central positional vetigo probably due to cerebellar in-farction is reported. The patient complained of positional vertigo and showed positional right-beating nystagmus when her head was tilted toward the left under Frenzel's glasses. The positional nystagmus was characterized by a lack of a latency period after moving to the provocative position and fatigability on repetitive stimulation. Electronystag-mography indicated direction-changing positional nystagmus: in the left-lateral position, there was nystagmus to the right and in the right-lateral position, nystagmus to the left. These findings suggested a central vestibular lesion. MRI demonstrated a small in-farction in the right cerebellar hemisphere. Furthermore, the eccentric rotation test showed an imbalance in otolith-ocular reflex. The results indicated that the central positional nystagmus was induced by a change in otolithic input under disinhibition of the otolith-ocular reflex due to a cerebellar lesion.
For focal diagnosis in patients complaining of vertigo and equilibrium disturbances, learning and evaluation of stabilograms using a neural network (NN) were conducted in healthy subjects and patients with labyrinthine and brain disturbances. Stabilograms were recorded with eyes open and closed for 60 seconds. Learning and evaluation of stabilograms were performed using a NN program developed by Anima corporation. The learning was practiced with stabilograms of healthy subjects and patients with lesions in the labyrinth and the brain. Using loaded NN formed by the learning, stabilograms of other healthy subjects and clinical cases were evaluated. Results of evaluation, such as generation ability of the loaded NN, were shown by a corresponding ratio. Correspondence showed that the lesions inferred from output values of the loaded NN corresponded to those indicated by clinical diagnosis. (1) On evaluation of stabilograms of healthy subjects and clinical cases, the cor-responding ratio was 75% in healthy subjects and 76% in clinical cases. (2) On evaluation of stabilograms of cases of labyrinthine and brain disturbances, the corresponding ratio was 72% and 67%, respectively. (3) On evaluation of stabilograms of healthy subjects and cases of labyrinthine and brain disturbances, the corresponding ratio was 60%, 46% and 60%, respectively. Learning and evaluation of stabilograms by the NN provide useful information for focal diagnosis in patients with vertigo and equilibrium disturbances.
This study was conducted to examine the changes in body sway induced by presentation of slant 60° visual angle and upright visual stimuli. In the preliminary experiment, participants observed an X-axis line, a Y-axis line or a cross-in upright or slant presentations. Results showed no increase in body sway under any conditions. In the main experiment, perspective stimuli constructed of lines by which observers perceived an extent of space or non-perspective stimuli by which they perceived a plane surface were presented. Results indicated that body sway increased only when the perspective stimuli were shown in the slant presentation. The results suggested that only presentation of slant figures which participants perceived an extent of space affects postural equilibrium.
The aim of this study was to evaluate the relationship between dysfunction of the vertebrobasilar hemodynamics and pursuit eye movements. We quantitatively assessed the vertebrobasilar hemodynamics by MRA and pursuit eye movements by the eye-tracking test (ETT) and optokinetic nystagmus (OKN) in patients with central vestibular disorders. Then, the relationships between MRA and ETT results, and between MRA and OKN results were statistically analyzed. The combined amplitudes of ab-normal spikes on ETT were significantly correlated with the degrees of stenotic changes in the vertebrobasilar systems, but OKN results showed no significant correlation. This finding suggests that smooth pursuit dysfunction is closely related to atherosclerotic events in the vertebrobasilar artery. Therefore, ETT may be a sensitive parameter to evaluate vertebrobasilar insufficiency.
In most cases, nystagmus develops as a physiological or pathological reflex. However, cases of voluntary nystagmus have been reported. A 14-year-old boy complained of several attacks of dizziness with nausea. He could induce voluntary nystagmus and demonstrated this to us. Since 9 year of age he has been able to induce nystagmus in frontal gazing. His nystagmus was pendular jerky. Amplitude was 5-10 degree and the frequency was 6-7 Hz. Nystagmus could be sustained for more than 1 minute. The nystagmus did not diminish and was not limited by fatigue. We observed no nystagmus in gazing. Neither positional nystagmus nor positioning nystagmus was noted. Although the horizontal eye movement was slightly saccadic, the vertical eye movement was smooth. Optokinetic nystagmus was not well developed and showed partial inversion. Convergence was possible and latent nystagmus was not observed. Nystagmus as assessed by a caloric test was well developed. No abnormal neurological findings were indicated and MRI imaging revealed no lesion. Since William's first study was reported in 1865, many cases of voluntary nystagmus have been documented. Voluntary nystagmus is usually described as being of a high frequency and low amplitude. The duration is brief, less than 30 seconds, and limited by fatigue. In most cases, nystagmus is pendular and is sometimes jerky. We divide cases of voluntary nystagmus, which were examined by an optokinetic nystagmus (OKN) test, into two groups. One group showed a normal OKN pattern, which was described as typical voluntary nystagmus, and the other group showed an abnormal OKN pattern similar to congenital nystagmus. Our case was classified in the abnormal OKN group. In this case, nystagmus which is usually latent develops when the patient cannot control his eye movements or when he does so voluntarily.
A 64-year-old man developed bilateral exotropia in the primary position after a stroke. CT revealed bilateral thalamic infarction. The saggital view of MRI disclosed that the lesion extended from the thalamus toward the rostral portion of the mesencephalon, in the territory of the paramedian thalamic arteries. Occlusion of these arteries may cause bilateral paramedian thalamic infarction, because these arteries arise from a common trunk of the basilar communicating artery which then bifurcates. Clinically, bilateral paramedian thalamic infarction is characterized as the following triad; hypersomnolent apathy, amnestic syndrome, and vertical gaze paresis. This patient, however, was awake and had no memory disturbances. He was unable to adduct both eyes in lateral gaze, although adduction palsy could be overcome by covering the contralateral eye. Upward gaze was completely impaired, while downward gaze was limited in both eyes. Vertical oculocephalic maneuver elicited vertical eye movement and Bell's phenomenon was preserved. Convergence was absent. These combined supranuclear horizontal and vertical gaze palsies were attributed to the rostral mesencephalic lesion, including the rostral interstitial nucleus of the MLF, posterior commissures and interruption of cortico-pontine pathways to the paramedian pontine reticular formation (PPRF).