Development of balance functions in infants and children can be delayed for various reasons. However, there are three major causes unless particular neurological problems are associated with the delay. These three major etiologies are congenital vestibular loss, congenital blindness and mental retardation. In infants and young children, vestibular loss is assessed by electronystagmography recordings by the damped rotation test, but not by the caloric test. The damped rotation test in infants and children with congenital vestibular loss, shows very poor rotational nystagmus, but in infants and children with congenital blindness only or mental retardation only, the test shows normal rotational nystagmus. Normal children initially begin walking at approximately 12 months of age, but children with these problems frequently begin walking after two years of age. Because vestibular and visual information converge in the cerebellum, it is speculated that this contributes to the delay in the development of balance functions in infants and children with congenital vestibular loss or blindness. However, mental retardation may influence overall development. Development of balance functions can be delayed by various causes, and careful examination is required.
Horizontal variant of benign paroxysmal positional vertigo (hBPPV) was compared with conventional vertical BPPV (vBPPV) with regard to clinical features and findings of eye movement. Of 147 BPPV patients who consulted our clinic between January 1991 and April 1994, 11 patients showed nystagmus only when rolled on the plane of the horizontal semicircular canal (HSC). None of the 11 hBPPV patients later developed disorders of the central nervous system. When positional nystagmus was provoked in the recumbent position, laterality of the strength of nystagmus was observed in eight, latency in four, and fatiguability in five of the 11 patients. The nystagmus was geotropic in eight patients, whereas the other three showed apogeotropic nystagmus. Spontaneous reversal in the direction of nystagmus (second phase) was not observed. Of the seven patients who underwent caloric testing, four showed canal paresis. hBPPV and vBPPV showed similar distributions by gender and by past medical history. In age distribution, hBPPV and vBPPV had peaks in the 40's and the 60's, respectively. Although the difference was not significant, the incidence of canal paresis was higher in hBPPV than in vBPPV, which may suggest some HSC pathology in hBPPV.
Isolated living vestibular sensory cells are capable of self movement. This study was designed to demonstrate the motile response induced by acetylcholine. After application of acetylcholine, there was no change in cell shape observed, but after application of both physostigmine and acetylcholine, cell shape changed mainly in the infracuticular region. This response was completely blocked by atropine. The localization of F-actin in isolated vestibular hair cells was investigated using FITC-labeled phalloidin. In freeze-fixed vestibular hair cells, strong labeling was found in the hair bundle, cuticular plate and throughout the cytoplasm. Not only after application of both physostigmine and acetylcholine but also after applying acetylcholine alone, the labeling in the cuticular plate was reduced. Changes in this phalloidin labeling pattern suggest that actin could be involved in the basic mechanism of self movement of vestibular sensory cells.
In patients with Meniere's disease accompanied by cluster attacks of vertigo, the evaluation of treatment is different when the number of attacks in a cluster are counted or when a cluster is counted as one spell. To determine the appropriate management of cluster attacks of vertigo, 120 patients with confirmed Meniere's disease were examinined. They were 58 males and 62 females, and the average patient age was 46.0. Cluster attacks of vertigo had occurred for six months prior to treatment were classified into four patterns based on the frequency of attacks in a cluster, namely daily, twice a week, once a week, and twice a month. The following items were investigated, (1) the frequency, (2) the relation between frequency and period, and (3) the average frequency of vertigenous attacks per week in a cluster. We concluded that when evaluating the effects of treatment on vertigenous spells, we should make a distinction between a cluster and an ordinary definitive attack, and the definition of frequent vertigenous attacks in a cluster was more than twice a week. The Cluster Coefficient was calculated from the total number of clusters and the average frequency of vertigenous attacks per week in all clusters. The formula of the Cluster Coefficient expressing the effect of treatments on clusters should equal the numeric value.
Between 1990 and 1995, vestibular neurectomy was performed in 14 patients with Meniere disease or other peripheral vestibular disorders. Acute symptoms after neurectomy subsided within two weeks. Long term-results of vestibular neurectomy were evaluated from results of a questionnaire regarding handicaps in daily life. Responses were collected from 12 patients more than 2 years after the surgery. Physical or functional restrictions were reported by 8 to 16% of the patients. Psychological handicap was also reported by 8 to 16% of the patients. Questions regarding auditory function revealed the same tendency. However, 11 of 12 subjects indicated satisfaction with the results of vestibular neurectomy. Although this procedure is considered the most effective surgery for vertigo attack, a small percentage of patients felt some restrictions in daily life.
The vestibular cortex is speculated to be involved in the perception of self-motion due to labyrinthine stimulation. In this study, we hypothesized that patients with lesions involving the vestibular cortex would show vestibular agnosia, and that nystagmus-sensation dissociation, which is demonstrated by brisk caloric nystagmus without simul-taneous sensation of vertigo, would be a feature of vestibular agnosia. We used singlephoton emission computed tomography (SPELT) to measure regional cerebral blood flow (rCBF) in two cerebrovascular patients with nystagmus-sensation dissociation. Both patients had ischemic lesions involving mainly the right parieto-temporal lobe. It is suggested that the parieto-temporal lobe contains the vestibular cortex.
Time course studies of audiologic threshold by auditory brainstem response (ABR) and nystagmus by electronystagmography (ENG) were performed in guinea pigs actively sensitized with dinitrophenyl (DNP)-ascaris (72-hour PCA titers of more than 640) and specifically challenged with DNP-Bovine serum albumin (BSA) injected through the stylomastoid foramen. A significant threshold increase on ABR was observed 1, 10, and 24 hours after the antigen challenge. The threshold was back to the prechallenge level 7 days later. Nystagmus was observed in 15 of 21 animals within three minutes after an-tigen challenge. Hearing loss and nystagmus induced by antigen challenge in actively sensitized guinea pigs were similar to the findings in passively sensitized animals in our previous study. These results suggest that an actively sensitized animal model may be useful for repetitive antigen challenge.
Downbeat nystagmus in primary position usually reflects lesions in the posterior fossa near the cranio-cervical junction such as Arnold-Chiari malformation (type I). It is said that about one third of the patients with this sign have a Chiari malformation. However, the pathophysiological mechanism of downbeat nystagmus remains controversial. Several lesions responsible for downbeat nystagmus have been proposed, such as that in the medulla or cerebellum (flocculus, nodulus). In this study, the electrically elicited blink reflex was investigated in 6 patients (one male, five female, average age 53.3 yr.) with Arnold-Chiari malformation (Type I) presenting with downbeat nystagmus to evaluate brainstem function. Latencies of each components were in the normal ranges in all 6 patients; R1 (11.13+0.66 ms), ipsi-R2 (32.45+4.47 ms), and contra-R2 (33.98+5.09 ms). In addition, there were no abnormalities in any component of ABR in any patients. Eye tracking test (ETT) showed a saccadic pursuit pattern, especially downward. The frequencies of horizontal optokinetic nystagmus were preserved, whereas slow phase velocities were relatively decreased. Caloric nystagmus could not be suppressed during gaze in the visual suppression test. From these findings we concluded that downbeat nystagmus in Arnold-Chiari malformation may be due to cerebellar (flocculo-nodular) lesions, rather than medulla lesions.
To evaluate the usefulness of Magnetic Resonance Imaging (MRI) in the diagnosis of vertebro-basilar insufficiency (VBI), 32 patients with vertigo or dizziness who were suspected of having VBI and 19 patients with Bell's palsy (as control) were examined by MRI. Seventy-two percent of the VBI group and 16% of the control group showed asymmetry or bilateral narrowing of caliber of vertebral artery, the rate being significantly higher in the VBI group. Thirty-eight percent of the VBI group and 11 % of the control group demonstrated lacunar infarction in the brain stem and 69% of the VBI group and 32% of the control group demonstrated lacunar infarction in the basal ganglion, the rate being significantly higher in the VBI group. These MRI findings may contribute to the diagnosis of VBI.