Motion sickness is induced by unusual patterns of spatial information input, but not by a simple strong acceleration. Thus, in the process of the development of motion sickness, the disturbance of spatial orientation is noticed somewhere in the brain, leading to the expression of autonomic signs and symptoms. What part of the brain plays this key role? Peripheral vestibular input has repeatedly been proven to be necessary for motion sickness, even for visually-evoked motion sickness. The vestibular nucleus in the brain stem where spatial information including visual and somatosensory as well as vestibular inputs converge, is the primary candidate for this key structure. In the higher brain, the limbic system, particularly the amygdala, is another candidate. In our rat animal model, bilateral amygdala lesions significantly suppressed motion sickness signs, whereas hippocampus lesions did not. Using cFos protein expression as a marker for neuronal activation, we also showed that the central nucleus of the amygdala was activated by vestibular information during the hypergravity stimulation that induced motion sickness in rats. Involvement of the amygdala may explain some characteristic features of motion sickness, such as its diversity of signs ranging from sympathetic to parasympathetic, and its conditioned occurrence where by some susceptible persons become sick even in motionless vehicles.
Using dichotic sound, the effects of optokinetic vertical stimulation on the orientation of horizontal sound lateralization was investigated in 10 healthy subjects. Subjects were given vertical optokinetic (OK) stimulation, and interaural time differences (ITD) and interaural intensity differences (IID) were discriminated, respectively. At a light stripes velocity of 90°/sec, the amplitudes for the ITD discrimination tests during OK stimulation were significantly greater than those before the beginning of OK stimulation, those at a light stripes velocity of 30°/sec, and those at a light stripes accelerated velocity of 4°/sec2 (P<0.05). On the other side, at a light stripes velocity of 90°/ sec, the amplitudes for the IID discrimination tests during OK stimulation were only significantly greater than those at a light stripes accelerated velocity of 4°/sec2 (P<0.05). The median line of amplitude for both ITD and IID discrimination tests did not shift at a light stripes velocity of 30°/sec, 90°/sec, and 4°/sec2. The present study demonstrated that sound horizontal lateralization sensitivity may be influenced by vertical OK stimulation. These findings also suggest that horizontal sound lateralization is more dependent on high-speed vertical OK stimulation than low-speed vertical OK stimulation. Therefore, we hypothesized that there is some interaction between the subcortical pathway of high-speed vertical OK stimulation and the sound lateralization pathway. The results of the present study will help in the understanding of space perception, comprising multiple sensory inputs.
To clarify the effect of head motion on dynamic visual acuity (DVA), we analyzed the relationship between DVA and eye movements during sinusoidal passive head translation at 0.6-1.4 Hz (amplitude: 5 cm) along the inter-aural axis using our original linear sled. Five healthy subjects were asked to read aloud sets of three numbers presented on a CRT monitor at a 30 cm distance that moved sinusoidally at the same frequency (amplitude: 7.5 cm) in the opposite direction to the head. We evaluated the percentage of correct answers as an index of DVA. For comparison, control experiments were conducted while the head was stationary. The main results showed that DVA improved significantly during head translation compared to when the head was stationary at 1.4 Hz (paired t-test, p<0.05). Although head translation did not affect DVA at 0.6-1.2 Hz. At 1.4 Hz, the vestibuloocular reflex evoked by head translation increased tracking gain, decreased phase-lag, and suppressed catch-up saccades. Consequently, gaze velocity (eye velocity in space) was bigger with head translation versus a stationary head. In addition, we identified another DVA-determining factor that was independent of head translation and eye movements. We consider that these composite factors improve DVA during higher-frequency head translation.
Equilibrium function, psychological tests, and a questionnaire about orthostatic dysregulation were investigated in 103 patients who visited the laboratory of equilibrium function in Kumamoto University hospital from April 2004 to December 2005. The percentage of patients with autonomic nerve dysfunction comprised 42.7% of the total patients. Most (94%) of the patients with autonomic nerve dysfunction presented with orthostatic dysregulation. The patients with autonomic nerve dysfunction and orthostatic dysregulation showed several diagnoses by the equilibrium function test: peripheral vestibular disorders (37%), disease of the central nervous system (28.6%), abnormal blood pressure (75%), psychogenic disorders (100%), and origin unknown (14.3%). Tofisopam was effective in 60% of the patients with autonomic nerve dysfunction and orthostatic dysregulation. In the other patients, only 18.5% were naturally cured without medication. There was a significant difference between the group of patients treated with Tofisopam and a control group without medication. Tofisopam tended to be effective in patients whose blood pressure decreased by the schellong test. We consider that it may be possible to improve the curative effect on vertiginous patients by performing psychological tests and questionnaires about orthostatic dysregulation, adding to the routine equilibrium function tests including the schellong test.
Charcot-Marie Tooth (CMT) diseases is a clinically and genetically heterogeneous group of peripheral nerve disorders characterized by distal muscle weakness and atrophy. There have been some reports of CMT diseases with CNS involvement, especially cerebellar atrophy. Recently, families with CMT type muscular atrophy with cerebellar ataxia have been increasingly reported, and it has been proposed as a new disease entity. However, the pathogenesis of CMT diseases with CNS involvement is unknown. We reported eye moments recorded electro-oculographically in seven patients with Charcot-Marie Tooth diseases. Brain MRI demonstrated slight cerebellar atrophy in only one case and no apparent abnormality in the other six cases. No abnormal eye movement was found in two patients with CMT type 1, but some abnormal eye movements were surprisingly observed in five patients including one with CMT type 1, three with CMT type 2, and one with HNPP. The observed eye movement abnormalities were lateral-gazed nystagmus in 2 patients, impaired smooth pursuit in 5 patients, saccadic hypometria in 3 patients, and a decrease of saccadic velocity in 2 patients. In all 5 patients, decreases in the slow phase of OKN and of visual suppression on the caloric test were observed. From eye movements, three cases were diagnosed as cerebellar involvement, one as cerebellar and brain stem involvements, and one as suspicious cerebellar deficit. One patient with CMT type 1 showing cerebellar and brain stem involvements and abnormal eye movement was genetically diagnosed as CMT 1A, which is the most common form of CMT disease. The findings suggest that CMT disease with cerebellar or brain stem involvement is more frequent than has been previously reported. Further investigation is necessary on eye movement abnormalities in patients with CMT disease. Examination of eye movement was a very useful and sensitive indicator in the screening of CMT patients to evaluate any central nervous deficit, especially concerning cerebellar and brainstem involvements.