The history of radiodiagnosis of acoustic tumors (AT) is reviewed in this paper. Plain Xray films and tomograms of the internal auditory canal provided information suggesting the presence of AT, but the direct visualization of AT became possible after the introduction of posterior fossa myelography. Using this method, W. House and his group did splendid work in the early diagnosis of AT in the 1960s and 1970s. Pneumoencephalographic roulette tomography introduced in 1968 was also a useful method of visualizing these tumors. These methods, however, required a spinal tap and the injection of contrast material (Pantopaque or air), and these disadvantages prevented them from becoming routine clinical examinations. CT Scan-ning introduced by Hounsfield and Ambrose in 1973, was less invasive and provided a clear image of AT. However, an AT less than 1.5 cm in diameter could not be visualized. CT Scanning apparatus was further improved and diagnosis of intracanalicular tumors became possible with the third generation apparatus which can image thin section (1 to 2 mm in slice thickness). Although air CT cisternography, intro-duced by Sortland (1979), provided a clearer view of small tumors, the necessary injection of air into the subarachnoid space was a disadvantage, and a less invasive method was sought. Magnetic resonance imaging (MRI) is non-invasive, but a small tumor could not be detected with the earlier MRI with its normoconductive magnet. However, MRI with a superconductive magnet provides by far the clearest image of AT regardless of the size of the tumor. This new MRI apparatus is now widely distributed throughout the country and will greatly contribute to the early diagnosis of AT.
Eleven patients with bilateral loss and 14 with unilateral loss of caloric response were examined clinically. The patients with bilateral loss had more frequent vertigo attacks than did those with unilateral loss. Ten patients (91%) with bilateral loss and five patients (36%) with unilateral loss had bilateral sensorineural hearing loss. Five patients (45%) with bilateral loss showed "vestibular recruitment", and the caloric response of these patients fluctuated. Only one patient (7%) with unilateral loss showed "vestibular recruitment".
Posturography (PG) and integrated electromyography (EMG) were recorded simultaneously and their inter-dependence was examined. Surface electrodes were placed on the skin over the triceps surae bilaterally because these muscles control the center of foot pressure to maintain stability in the standing position. Electro-myograms were integrated with a time constant of 0.1 sec. Two oscillations, one from PG and one from integrated oscillations of EMG, were correlated. As long as body sway was limited to a small area, the two waves showed no correlation. However, with larger body sway, the correlation was higher. Oscilations in the antero-posterior (A-P) direction showed the highest correlation of PG and EMG. On the other hand, when oscillations were in the right-left (R-L) direction the correlation of PG and EMG was lower. These findings indicate that A-P oscilla-tion and R-L oscillation are independent in PG in the standing position. The positive correlation between PG and EMG implies that the pivot of body sway is in the ankle joint. These findings support the theory that body sway oscillation resembles that of an inverted pendulum.
A 63-year-old male complained of vertigo and bilateral sensory hearing loss and then developed relapsing polychondritis. Cases of relapsing polychondritis with vertigo as the initial symptom are rare: only 4 have been reported in Japan. Otoneurological tests revealed bilateral sensory hearing loss and bilateral canal paralysis. Corticosteroid hormone therapy markedly improved his left hearing level and left canal paralysis. It is thought that the vartigo in this case was caused by relapsing polychondritis related to auto-immune reaction to type II collagen.
The influence of pendular head rotation on optokinetic nystagmus was studied with the use of a pendular rotating chair and an optic cylinder operated independently. Healthy subjects and patients with unilateral loss of vestibular function were examined. The pendular rotation and optokinetic stimuli were applied in both horizontal and vertical directions. The optokinetic stimuli consisted of 12 stripes rotating with applied uniform velocity of 90°/sec. The pendular rotation was applied at a frequency of 0.1 Hz and a peak angular velocity of 30°/sec. In healthy subjects, horizontal optokinetic nystagmus was promoted when the head rotated to the direction opposite to the optic cylinder rotation. On the other hand, when the head and optic cylinder rotated in the same direction, optokinetic nystagmus was inhibited. In patients with unilateral loss of vestibular function, a difference in response to ampullopetal and amupullofugal stimulation of the remaining intact labyrinth was seen. However, this difference gradually disappeared with compensation. In healthy subjects, vertical pendular rotation promoted and inhibited vertical optokinetic nystagmus. In patients with unilateral loss of vestibular function, promotion by vertical pendular rotation of vertical optokinetic nystagmus was the same as that in healthy subjects. The influence of active pendular head rotation on optokinetic nystagmus was studied with an optic cylinder fixed to the head. Inhibition of nystagmus during active pendular head rotation was weaker than that during passive pendular head rotation, but the effect on promotion was almost the same.
A cerebellopontine angle lipoma was found in a 52-year old female. The patient suffered from vertigo and left hearing loss, but no episode of tinnitus or fluctuating hearing loss. Neurological examinations revealed left hearing loss, decreased caloric reaction on the left, increased of -SP/AP on left EChoG and prolongation of I-V inter peak latency on the left ABR. A review of the literature on 24 cases of cerebellopontine angle lipomas found during surgery suggests that these lipomas cause a combination of the symptoms of Meniere's disease and of acoustic neuroma.
All the subjects in this study were over 65 years of age. Twenty one healthy persons with-out vertigo attacks and 167 patients with vertigo attacks and with unsteadiness were examined. Neurotological examinations were performed, and body balance was determined by recording of the gravity center. 1 The length and area of the movements of the gravity center in the healthy subjects over '65 years of age were greater than in 20-50 year-old healthy subjects. 2 The average of the length and area of the gravity center movements in patients with inner ear lesions and dizziness were within normal limits in patients over 65 years of aye. 3. The results of examinations using gravity center movements should be confirmed by mental calculation during stabilometry. When the length and area of the gravity center movements in patients complaining dizziness are remarkably larger, the results should be confirmed by duplicate examinations and by the examinations with mental calculation.
A 34-year-old female with positional vertigo and nystagmus had been misdiagnosed as having benign paroxysmal positional vertigo because of the positional nystagmus with latent period and decrescence and the absence of hearing loss and of neurological symptoms during attacks of vertigo. However, MRI and CT-scans showed a cerebellar cavernous angioma. MRI and CT-scan are necessary in the diagnosis of the cause of vertigo even when it seems to be due to peripheral vestibular disease.
The endolymphatic sac blood flow in guinea pigs was measured by a laser Doppler method (Advance Laser Flowmeter, Model ALF 2100) following the intravenous administration of isosorbide. Under general anesthesia with intraperitoneal pentobarbital sodium, the occipital bone was removed and the posterior cranial fossa was exposed. After incision of the dura mater, the cerebellum was pushed to the left to visualize the right endolymphatic sac. A measuring probe was placed on the endolymphatic sac with the use of a micro-manipulator. During this experiment the respiration was controlled by a respirator and blood pressure was monitored. Isosorbide was administered intravenously through the jugular vein for 60 seconds. The endolymphatic sac blood flow increased immediately after administration, reached a peak within 3-4 minutes and decreased gradually to the initial level in 12-15 minutes. The endolymphatic blood flow changes almost always corresponded to the systemic blood pressure changes. The endolymphatic sac blood flow had almost the same pattern as the cochlear blood flow seen in our previous study done under the same ex-perimental conditions. In spite of the anatomi-cal differences in the vascular supply, these two inner ear portions showed almost the same responses to isosorbide.