The interpretation of ENG recordings in patients with an artificial eye has certain difficulties. The artificial eye moves in association with the intact eye, but the horizontal recording from the artificial eye is deflected in the opposite direction to the intact eye movement, synchronously and with minimum amplitude. This inverted horizontal deflection of ENG was first documented by Miles in 1939. However, the mechanism of this phenomenon remains to be elucidated. A subject with a left artificial eye and a right intact eye was selected for this study. Poly-graphic recordings were taken from several electrodes attached to the outer and inner canthus of the right eye, a, b; the nasal roof, c; and the inner and outer canthus of the left eye, d, e. The indifferent electrode was placed on the mastoid process. When the test subject was asked to gaze at a target 30° to the left, a showed -107.6μV; b, 124.3μV; c, 78.9μV; d, 57.2μV; e, 12.1μV. When he gazed 30° to the right, a showed 122.1μV; b -99.2μV; c, -63.3μV; d, -43.3μV; e, -29.5μV. Those data were well predicted by the electrical potential induced by movement of the intact eye alone. These results were compared with those of two normal subjects and two patients with oculomotor palsy. It was concluded that the synchronous inverted horizontal ENG recording from the artificial eye is caused by movements of the intact eye. It is assumed that the field of potential in one eye is always influenced by the corneoretinal potential of the other eye.
The statokinesigrams of 16 patients with benign paroxysmal positional vertigo (BPPV) and of 13 with vestibular deficits (VDS) were compensated with those of 20 normal subjects (NS). Velocity of the track (LNG/T), root mean square (RMS) and standard deviation area (SD-Area) were used as parameters. Fourteen different tests were performed (Table 1). There were interesting differences between the compensated VDS and BPPV patients and between the untreated period and the compensated stage in each patient group (Table 3). In the compensated stage, the BPPV group was less stable than the NS while watching LED with OKN on the tactile information plate (S-G plate). The differences in RMS and SD-Area were significant. The data for the NS and the untreated VDS group showed that the latter was more unstable while watching LED with OKN than in the dark on the S-G plate. The compensated VDS group was more unstable than the NS during OKN or while watching LED which was almost the same as in the dark on both plate conditions, and more unstable while watching LED than during OKN on the S-G plate. The differences in velocity of body sway (LNG/T) were significant. The neural region for compensation in BPPV patients might be on the visuo-oculomotor pathway through the peripheral retina. One of the most important region for compensation in VDS patients might be in the rhombencephalic reticular formation.
Brain stem pause neurons (PNs) have been reported to play important roles in the regulation of rapid eye movements. However, the input sources that drive PNs are uncertain. The present study indicates monosynaptic connections from vestibular Type I and Type II neurons in the medial and lateral vestibular nuclei to the PN region. This conclusion is based on (i) antidromic activation showing vestibular neurons projecting to the PN region ; (ii) systematic microstimulation tracks within the PN region showing a depth-threshold pattern of antidromic activation of vestibular neurons consistent with vestibular neurons having profuse axonal branches within the PN region ; and (iii) spontaneously firing single vestibular neurons evoking a spike-triggered field response in the PN region.
In order to know the point of action by galvanic stimulation, galvanic body sway and caloric test were done in the patients whose parts of lesion were evident by operation or other method. The results were as follows : 1. Patients with inner ear disorders showed normal galvanic body sway (GBS) and decreased caloric response. 2. Most of patients with the lesion of vestibular nerve and Scarpa's ganglion showed abnormal CBS and caloric response. However, three of them showed discrepancy between CBS and caloric response. From these results, we suspected that the part of action by galvanic stimulation would be the afferent fiber from the otolith system. 3. Three patients with brain stem lesions showed normal GBS and caloric response.
The CMI test was performed to clarify the predisposition of patients with vertigo. 1. CMI III and IV types were noted in about 30% of patients with vertigo. They showed neurotic tendency. CMI IV type was noted in none of patients with Ménière's disease or benign paroxysmal positional vertigo (BPPV). They showed psychiatric stability. 2. Patients with vertigo showed high scores for the Eyes and ears and the Habits. It was thought that the former was the predisposition to onset of vertigo and the latter was the cause to onset of vertigo. The scores for physical and psychological symptoms showed no difference between Ménière's disease and BPPV. Patients with otogenic vertigo showed high scores for psychological symptoms and psychiatric instability. 3. The Anger of 9 specific psychiatric items was characteristic of patients with vertigo. It was concluded by individual interviews that the Anger was equivalent to emotional instability.
Gaze stabilizing function during active head rotations at high frequencies was investigated in 12 normal adults. Head rotation amplitude decreased as the frequency increased, from 31° at 2 Hz to 11° at 5 Hz on average ; the corresponding maximum head velocity and acceleration amounted to about 170-200°/sec and 2500-5000°/sec2, respectively. At the frequencies higher than 2 Hz, the amplitude of compensatory eye movement exceeded head rotation amplitude ; the mean ratio of the former to the latter increased linearly from 1.19 at 2 Hz to 1.80 at 5 Hz. The present study indicated that the compensation for head rotation by the vestibulo-ocular reflex, which is adapted in daily experienced head movements, deteriorates quickly as head oscillates over this functional range.
The operative findings of traumatic vertigo were studied in 65 patients who had surgery for middle ear trauma. A complaint of vertigo was present in 23 patients and absent in 42. A perilymphatic fistula was found in 19 patients with vertigo and 2 patients without vertigo. The incidence of perilymphatic fistula was correlated with the accompanying symptoms. There was no positive correlation with loss of consciousness, or temporal bone fracture or ossicular dislocation, but there was a positive correlation with the way the traumatic force acted on the inner ear windows. Vestibular function tests in the 19 fistula patients with vertigo showed positional nystagmus in 12 cases and a fistula sign in 10 cases. These two tests are considered to be important in the diagnosis of perilymphatic fistula.
Quantitative eye movement recordings in a patient with spinocerebellar degeneration who had macrosquare wave jerks and macrosaccadic oscillations showed the mechanism of macrosaccadic oscillations. Macrosquare wave jerks show square waves, but macrosaccadic oscillations show spindlelike waves on recording papers. Both saccadic eye movements had intersaccadic intervals. The relationships of amplitude-maximum velocity of saccades, macrosquare jerks and macrosaccadic oscillations were normal. Macrosaccadic oscillations on fixation and saccadic pursuit were the same in intersaccadic intervals and errors-amplitude of corrective saccade relationships. Observation of the intersaccadic intervals of macrosaccadic oscillations showed that the saccade following the first interval was a corrective saccade. Since the corrective saccade is hypermetric, however, the eyes oscillate. Finally the eyes catch the target by visual inputs. Neuro-otological examinations showed that this patient had disturbances of the cerebellar vermis, which controls saccadic eye movement. Thus, it was shown that macrosaccadic oscillations are caused by disturbances of the cerebellar vermis.
A 24-year-old, right-handed man with periodic alternating nystagmus (PAN) due to adrenoleucodistrophy was studied neuro-otologically. In this case, PAN was a comparative large horizontal nystagmus, containing a mild rotatory component, and the amplitude of the nystagmus first increased and then decreased in each span. An average cycle length of the PAN was 180 seconds with a right-beating phase of 95 seconds, a left-beating phase of 75 seconds and null periods of 5 seconds between each phase. The PAN was not affected by eye closure, state of darkness, changing direction of gaze, changing of head position, or the optokinetic nystagmus testing. However, the PAN continued for about 6 months and then gradually disappeared. CT-scan showed obvious generalized cerebellar and brain stem atrophy. On comparating this CT-scan with one done 6 months previously, there was a definite increase in cerebellar and brain stem atrophy.
A 21-year-old male college student had a spell of vertigo when he bumped his head against an opponent during American football drill on August 15, 1985. Severe vertigo subsided in 30 seconds but dizziness continued for several hours. On August 24, he was admitted to the Gifu University Hospital because he had an attack of vertigo when he got up in the morning. On the day of his hospitalization, spontaneous nystagmus to the right was observed. He was discharged asymptomatic on August 31. Since discharge, he had no attack of vertigo for about 1 year. On March 5, 1986, he felt rotatory vertigo lasting for about 30 seconds whenever he tackled during American football drill. On March 6, he visited our out-patient clinic. Neuro-otological examination revealed vertical rotatory nystagmus induced by head position change. CT showed a cyst in the cavum septi pellucidum and deviation of the basilar artery to the right. MRI and Metrizamide CT indicated distortion of the right vertebrobasilar artery and compression of the brainstem. Right vertebral angiography showed a tortuous vertebral artery. It was concluded that the vertigo was due to lower brainstem disturbances caused by vertebrobasilar insufficiency. The patient was advised to discontinue American football. At present, he is free from vertigo.
The frog utricle and its nerve were isolated with the anterior and the lateral semicircular canal ampullae in frog Ringer's solution. The utricular otoconia and the otoconial membrane were carefully removed. The cupula of the anterior semicircular canal was removed and was sectioned in half. The halved cupula was stuck into the tip of a glass microelectrode which was mounted on a micromanipulator. The base of the cupula was gently placed on the macula. The micromanipulator allowed sliding motion of the cupula on the macula. The cupula was placed in the center of the medial or lateral part of the macula and was moved toward (striolapetal) or away from (striolafugal) the striola along the axis vertical to the striola. When the medial part of the macula was stimulated, 5 μm of striolapetal cupula movement elicited excitatory nerve discharge. When the lateral part of the macula was stimulated, the striolapetal stimulus likewise induced an excitatory response. These results indicate the presence of physiological polarity on the utricular macula.
The body sway test is the most useful assessment of vestibular dysfunction. We compared 24 normal subjects and 44 patients with unilateral Ménière's disease. The time course of Ménière's disease was also evaluated by non-sequential vector analysis after endolymphatic sac operation. Body sway in normal subjects was usually dominant in the right-forward to left-backward direction and always more so in patients with Ménière's disease with eyes open or closed. This analysis was useful in evaluating the time course of Ménière's disease and effect of endolymphatic sac operation.
1) The data published by the Welfare Ministry and the Gifu prefectural office were analyzed with respect to persons with balance disorders. Balance disorders account for only 0.1 percent to 0.2 percent of all physical disabilities. 2) The number of, persons with balance disorders living in Gifu prefecture is 81. 3) The causes of the balance disorder in these 81 persons were : labyrinth or eighth cranial nerve damage (31), CNS disturbance (42), combined disturbance of the labyrinth and CNS (4), and unknown (4). 4) Persons under 18 years or 60 years of age had mainly CNS disturbances. 5) The incidence of multiple handicaps, especially balance disorder plus deafness, was higher in the labyrinth and the eighth cranial nerve damage group than in the CNS disturbance group. 6) Grade 5 balance disorder was more common than grade 3 in the labyrinth and the eighth cranial nerve damage group. The number of grade 3 and grade 5 balance disorders was approximately equal in the CNS disturbance group.
Five patients with episodic vertigo, tinnitus and hearing loss were found to have compression of the eighth cranial nerve by small aneurysm or arterial loops. The characteristic symptoms in these patients were : 1) Short term and sudden-onset vertigo occurring frequently and not responding to medical treatment. 2) Patients became asymptomatic immediately when the attacks ended. 3) Hearing loss fluctuated widely but briefly at low or wide frequency ranges. 4) In some cases there were associated ipsilateral facial spasms and/or trigeminal neuralgia. 5) Nausea and vomiting during the vertigo attacks were less prominent than with Ménière's syndrome. 6) Severe and frequent attacks were observed even, in patients with severe semicircular canal palsy. 7) Vertebral angiography showed elongation and enlargement and sharp angulation of the fourth segment of the vertebral artery on the affected side.
Twenty-eight patients (30 ears) with Ménière's disease were treated by intratympanic injection of 4% Lidocain. Lidocaine (0.5 ml) was infused into the tympanic cavity transtympanically. These patients had been treated by other conservative medical therapy for at least one month, but had not responded. Examination 6 months later showed that : 1) This method was extremely effective in reducing vertigo. In 24 ears (80.0%) the vertigo disappeared completely, in 2 ears (6.7%) it improved considerably, while in 4 ears it remained unchanged. 2) In 6 ears (20.0%) hearing improved to above 15 dB, and in 24 ears (80.0%) it remained unchanged. We did not find any deterioration of hearing after the therapy. 3) Before the injection all patients had tinnitus. Tinnitus was reduced in 9 ears (30.0%) with comparatively good hearing under 55 dB prior to therapy, but remained unchanged in the other ears. The intratympanic injection of 4 % Lidocaine is not only extremely effective but is also very safe as a therapy for Ménièr's disease. Therefore we consider this therapy worth trying for severe Ménièr's disease before more extreme surgery is considered.