To clarify the peculiarities of gait in elderly Japanese we used a gait test which consisted of qualitative and quantitative analysis of gross observations of free walking for 10 m recorded by pen oscillography on a polygraph of 7 phenomena : 5 of which with the aid of a five-channel telemeter, head movements (upward-downward, right-left, and forward-backward), activity of both soleus muscles, and bilateral foot-floor contact sequences. The power spectrum and correlation analyses were carried out with a PDP-11 computer. 1) In normal young adults, head movement recording revealed regular upward-downward movement and forward-backward inclination twice in each walking cycle and regular right-left inclination once in each walking cycle. Each soleus muscle was activated in the stance phase once in each walking cycle. 2) In the elderly, the rhythm of foot-floor contact and the smooth-reciprocal swinging of the arms in free gait were often more disturbed with age when the eyes were closed than when they were open. Time required for walking 10 m, step width, and inclination length tended to increase, while cadence and step length tended to decrease with age. 3) In the elderly, the irregular right-left and forward-backward sway often increased, and the pattern of soleus muscles activity during walking was irregular. These changes of free gait in the elderly are caused not only by aging changes of the skeleto-muscular structure but also by the effect of age on proprioceptive postural regulation.
Congenital nystagmus can be divided into five types : jerky, pendular, pendular-jerky, latent and periodic alternating. We examined 28 patients with congenital nystagmus from 1987 to 1992 and analysed the results of ENGs recorded with eyes open, eyes closed, eyes open in the dark and during eye tracking and optokinetic pattern testing. Eleven patients had jerky, 6 had pendular, 8 had pendular-jerky, 2 had latent, and 1 had periodic alternating nystagmus.
We compared the balance behaviour of 15 chicks hatched under 2 G with that of 14 chicks hatched under 1 G to investigate the influence of hatching under hypergravity on vestibular function. These two groups showed the same behaviour, so it seems probable that hatching under hypergravity produces scarcely any permanent disorder of vestibular function.
The maximum velocity of the slow phase of caloric nystagmus was mesured from the electronystagmograms of 354 patients with various kinds of inner ear disturbances. The percentages of canal paresis and directional preponderance were calculated according to Jongkees' formula. The authors set the normal limits of 'canal paresis' (CP) and of 'directional preponderance' (DP) at ± 26% and ± 29%, respectively. DP was found in28 patients and DP+ CP in 59. The calorigrams of these 87 patients were classified into three types : (1) Both caloric nystagmuses directed to the right side (induced by a hot stimulus on the right side and a cold stimulus on the left side) were larger than both caloric nystagmuses directed to the left side (induced by a hot stimulus on the left side and a cold stimulus on the right side) and vice versa (28 patients). (2) One caloric nystagmus directed to the right side (induced by a hot stimulus on the right side or a cold stimulus on the left side) was larger but the other caloric nystagmus directed to the right side (induced by a hot stimulus on the right side or a cold stimulus on the left side) was smaller than one or both of the two caloric nystagmuses directed to the left side (induced by a hot stimulus on the left side and/or a cold stimulus on the right side) and vice versa (46 patients). (3) Because of severe canal paresis on one side, one caloric nystagmus was much longer than the other caloric nystagmus on the unaffected side (13 patients).
We investigated the mechanism by which repetitive optic stimulation affects optokinetic responses. Eleven persons, physically healthy, took part in this study. The subjects were stimulated optokinetically to the right. The angular velocity of the Ohm type drum was 50 deg/sec, and the duration of the stimulation was 30 seconds. This stimulation was successively applied 5 times a day over a period of 3 weeks. Optokinetic nystagmus (OKN) was recorded with electronystagmography and analyzed with a computer. Before and during this trial, we did 2 tests every week. First, the drum was rotated with an angular acceleration of 2 deg/sec2, and optokinetic adaptation limit (OAL) was estimated. Next, the drum was rotated with an equal velocity of 40, 60 and 80 deg/sec. The initial rapid rise (IR), the maximum steady state slow phase velocity (SS) and the time constant of optokinetic afternystagmus (TC) were calculated. These items were evaluated with stimulation towards the right only in 5 subjects and with stimulation towards both the right and the left in 6 subjects. Optokinetic training produced the following results : OAL increased significantly on stimulation towards the right, but did not increase on stimulation towards the left. SS increased significantly at a velocity of 60 and 80 deg/sec in both directions. IR increased significantly on stimulation toards the right, and increased slightly on stimulation towards the left. TC decreased on stimulation towards the right. We conclude that the increase of the slow phase velocity of OKN was due mainly to the enhanced function of the pursuit system, but other factors also had a role in training effects.
To clarify the relationship between susceptibility to seasickness and the function of the vestibular system, we examined 35 healthy male students in the second year of Toyama Fisheries High School (16 or 17 years old) before and after their first voyage, using the bithermal caloric test and the pendular rotational test (0.05 and 0.1 Hz). The results of the two tests were correlated with the severity of sea sickness, duration of sea sickness and the number of vomiting episodes. Thirty-three of 35 subjects (94%) suffered from sea sickness. The mean duration of sea sickness was 5.3 days, and the mean number of vomiting episodes was 5.5. In both the number of beats and the maximum slow phase velocity of caloric nystagmus, a significant correlation was found between the pre-voyage test results and the difference between the pre-vs. post-voyage test results (p< 0.05). Furthermore, these two parameters in the pre-voyage test were significantly correlated with the duration of sea sickness (p <0.05). As for the rotation test, the pre-voyage VOR gain at the frequency of 0.05 Hz was significantly correlated to the difference in value in the pre-vs. post-voyage VOR gain (p< 0.05). No correlation was found between severity of sea sickness and either pre-or post-VOR gain (0.05 and 0.1 Hz). These findings suggest that the caloric test may be useful in predicting susceptibility to sea sickness.
The stages of continuous vertigo of peripheral origin were classified into nine categories according to the findings of spontaneous nystagmus (SPN) and head-shaking nystagmus (HSN). The patients analyzed were composed of 18 cases with vestibular neuronitis, 6 with sudden deafness and vertigo and 6 with inner ear disorders. 1) Irritative SPN (Stage I) was rarely seen. 2) SPN of the paralytic type (Stage II) was usually observed within one month after the onset of disease. 3) HSN directed towards the intact ear with or without a reversal phase (Stage III-2 and III-1, respectively) was the common type of central compensation. 4) In the process of recovery to complete cure (Stage V), HSN could disappear trasiently (Stage III-3), or be directed toward the affected ear without a reversal phase (Stage III-5). However, HSN directed toward the affected ear with a reversal phase (Stage III-4) was not observed. 5) Spontaneous recovery nystagmus (Stage IV) could also occur. 6) About 40% of patients recovered to Stage V within about 4 months after the onset of vertigo, but about 30% of patients remained in Stage III-1 or III-2 even 4 months after the onset of disease.
We studied six patients with palatal myoclonus (p.m.), two of whom had oculopalatal myoclonus (o.p.m.) and four p.m. only. We used Electronystagmography (ENG) and Auditory Brainstem Response (ABR) to compare them. In the two o.p.m. patients pontine hemorrhage was seen in the lateral brainstem in Brain CT scans. They had a decreased total slow phase velocity of OKN, prolonged latency of waves III and V, and disappearance of ABR after wave III. These findings indicate brainstem disturbances. Cerebellar and pontine lesions were seen in Brain CT scans of two. Three of the four patients with p.m. of the four had normal OKN but the other two had decreased total slow phase velocity. Two had a normal ABR, and the other two had prolongation of latency waves III and V. These abnormal findings must be caused by the fact that the relaying nuclei of the auditory brainstem passway are near the central tegmental tract in the Guillain Mollaret triangle. We conclude that ABR can be used as an aid to detect brainstem disorders that cannot be found by CT, MRI or OKN and can also exclude the possibility of cerebellar disorders.
Spontaneous abnormal eye movements are frequently caused by disease in the aqueduct of the midbrain and indicate the location of the lesion the at an early stage. We report here a case of Sylvian aqueduct syndrome in which neuro-otological findings became clues to the diagnosis. Our patient was a 54-year-old male with the chief complaint of unstable dizziness. He showed intermittent convergence nystagmus and upward gaze palsy. Hydrocephalus following non-tumoral aqueduct stenosis resulted in a lower inclination of the brainstem and caused such ocular symptoms. Structural changes could not be demonstrated in images at an early stage. Oculomotor abnormalties changed after a V-P shunt was placed and eventually disappeared.
In an effort to determine the mechanism causing motion sickness, various studies have been conducted on the autonomic and central nervous systems. Recently, it was reported that the level of antidiuretic hormone (ADH) rises when motion sickness appears, and the possible involvement of hormones in the manifestation of motion sickness has become a focus of attention. We induced motion sickness by Colioris stimulation in healthy adult volunteers, and examined hypothalamus-pituitary-adrenal hormones and neuropeptides before and after stimulation and during the recovery process. In the high susceptibility group blood levels of ADH, ACTH, prolactin, cortisol, β-endorphin and MET-enkephalin and urinary levels of ADH immediately after stimulation were significantly higher than those in the low susceptibility group. These levels returned to normal after 30 minutes of rest. In the high susceptibility group the motion sickness score immediately after stimulation showed a significant correlations with the blood levels of ADH, ACTH and β-endorphin. These results indicate that ADH, ACTH, β-endorphin and MET-enkephalin are involved in the nausea and vomiting of motion sickness. Moreover, it seems that the mechanism and effects of these hormones may differ from each other. Since the urinary level of ADH is very closely correlated with its blood level, the use of urinary ADH testing is advocated as a simple method with no discomfort.
A 54-year-old female with bilateral rapidly progressive hearing impairment, tinnitus and dizziness was sent to our ENT clinic. She also complained of headache and low grade fever. Pure tone audiometry showed bilateral severe sensori-neural hearing loss, and direction-changing positional nystagmus towards the upper ear side was observed. Neurological examinations revealed truncal ataxia and a positive Babinski's sign. Electronystagmography (ENG) and eye tracking test (ETT) showed saccadic pursuit and hypometric saccade; optokinetic nystagmus (OKN) and optokinetic after nystagmus (OKAN) were impaired bilaterally. Her serum TPHA titer was very high, so erythromycin was given orally in a daily dose of 1600 mg for 30 days. Her dizziness improved gradually, but hearing impairment progressed rapidly to bilateral total deafness. MRI revealed no significant lesion except a pituitary adenoma. We suspected that otosyphilis and positional nystagmus was induced by stenosis of the basilar artery.