Vestibular pathophysiology during vertiginous attacks was discussed on the basis of clinical observations and basic research, and was summarized as follows: 1) Essential differences between cochlear damage and vestibular damage were noted. Cochlear symptoms were signs of the affected side cochlea. However, vestibular symptoms were caused by functional imbalance of the vestibular organs between the affected side and the normal side. The process of disturbance in the vestibular organ on the affected side showed two different stages: first, irritation, then paralysis. However, in the cochlear damage, there was only a paralytic state without any sign of initial irritation. Investigation of these differences is very important to clarify the discrepancy between vestibulo-cochlear symptoms and inner ear pathology. 2) The labyrinth progressed through 4 states during the process of peripheral vertigo: a) the disturbed stage, b) the recovery stage, c) the compensatory stage, and d) the revival stage. Treatment for peripheral vertigo should be selected according to the state of labyrinth, and discrimination methods of the labyrinthine state were discussed.
Fifty-four nystagmus tests were performed under infrared camera in 39 patients with unilateral acoustic neuroma surgery. Equilibrium symptoms were evaluated subjectively by the patients using a questionnaire. Spontaneous and positioning nystagmus occurred less frequently as time passed after surgery. However, postoperative head-shaking nystagmus usually occurred in approximately 80% of the patients. Regarding head-shaking nystagmus, two types were observed, the one-phase type to the unaffected side and the two-phase type to the unaffected following the that to the affected side. Compensation for nystagmus after surgery was demonstrated for a long time. However, compensation for equilibrium symptoms evaluated by questionnaire showed a good prognosis. Regarding the relation between age and compensation for nystagmus and/or for equilibrium symptoms, younger patients showed better compensation.
Electrooculographically, head turn with eyes closed may induce transient saccadic eye deviation (TSD) in the direction of the head movement as a result of activation of the lateral gaze center driven by neck torsion. TSD during active head turn has shown an incidence of 100%, a mean angle of 32.8°and a mean velocity of 163°/sec. Latencies of TSD from head turns monitored by electro-myographic bursting on the splenii capitis muscle were measured and compared with the latency (mean value of 175 msec.) of voluntary saccadic pursuit for a 10°visual angle in 12 normal subjects (aged 26 to 57 years). The mean latencies and standard deviations in active and passive head turns were 36.5±10.4 msec. and 50.9±15.6 msec., respectively, showing a significant difference (P less than 0.02). The latter should be prolonged by antecedent small vestibuloocular reflex to TSD according to a lowered alertness of the parapontine reticular formation. In conclusion, the latency of TSD may be an indicator of alertness or functional disorders of the brainstem.
This study was performed to investigate the hemodynamics of the basilar artery (BA) of normal subjects and patients with vertigo by transcranial Doppler ultrasonography (TCD). There were 85 normal subjects, 50 males and 35 females, 23 to 83 years old (mean 50.0 years), and 74 patients with vertigo, 34 males and 40 females, 23 to 83 years old (mean 63.8 years). The mean blood flow velocity (FV) and Fourier pulsatility index (FPI) of the BA were measured by a midline approach. In normal subjects, FPI increased while FV did not change in the elderly. In patients with vertigo, FV decreased in 24 cases, FPI increased in 15 cases. Transcranial Doppler ultrasonographic evaluation is a feasible, noninvasive, reproducible technique that can detect abnormal hemodynamics in the BA.
The present experiment examined the influence of asphyxia on neuronal activities of the primary vestibular neurons in guinea pigs. These results were obtained as follows: 1. During asphyxia, spontaneous firing in a total of 33 units analyzed disappeared with or without transient increase of discharges. 2. Recovery of discharge was seen in 6 units (18%) within 3 minutes. 3. Increments of firing rates during asphyxia were larger in irregular and intermediate firing units than in regular units.
The pathogenesis of vertebro-basilar TIA is regarded to be stenosis or obstruction of the vertebro-basilar artery, hemodynamic factors, and microemboli. This report deals with neurotological findings in vertebro-basilar TIA (V-BTIA) on circulation and imaging studies. Neurotological testing was used to evaluate circulation in the vertebro-basilar artery in 31 patients with V-BTIA who consulted our clinic in Nara Medical University Hospital between 1992 and 1994. On neurotological findings, static and kinetic body balance test show normal results, and test of labyrinthine reaction also show normal findings. On circulation test, however, ECD (extracranial doppler test) and TCD (transcranial doppler test) detected abnormal findings in many patients. On imaging study, pathological lacunar infarction was detected on CT and MRI in some patients, and also kinking and coiling in the vertebral artery in MR angiography. We have concluded that V-BTIA orginates from hemodynamic factors rather than vascular factors considering the pathogenesis of vertebro-basilar circulation.
A behavioral study was performed to examine the effect of glucocorticoid agonist (dexamethasone) and glucocorticoid receptor antagonist (RU38486) on the vestibular compensation following unilateral labyrinthectomy in pigmented young rabbits. The frequency of spontaneous nystagmus and the angle of head deviation were both reduced markedly in the rabbits treated with 1 or 5 mg/kg intravenous dexamethasone compared with the controls treated with saline. In contrast, intramuscular RU38486 retarded improvement of the vestibular symptons. These results suggest that endogenous glucocorticoids contribute to the achievement of the vestibular compensation.
Morphometric observation and evaluation consisting of celloidine serial sections, a microscope with a drawing tube, an image analyser and a computer are necessary for the precise understanding of the morphological development of the human nervous system with great objectivity. We introduced this method and particular anatomic parameters such as the circularity ratio (CR) and neuropil index (NI) with the preliminary data of the vestibular nuclei at 40 weeks of gestation (WG). For the analysis of the maturity of neurons, CR of neuronal somata, 47πA/L2 (A=area in um2; L=perimeter in pm), was calculated. The CR of a regular circle is 1.0. We evaluated the maturation of the neuropil defined as the tissue around each neuron including the axons, dendrites, myelin sheaths, glial cell bodies and their processes, vessels and connective tissue. The NI was calculated as follows: NI=[(total columnar area in mm)-(total neuronal area in mm)] X 103/neuronal number; We measured sections to obtain several morphometric parameters: the volume of the nuclear column, and number, packing density and cell body area of neurons, and calculated CR and NI, demonstrating the value at 40 WG. We are currently preparing to examine the development of the human lateral vestibular nucleus in 14 fetuses (6-40 WG), an infant (2 months old) and an adult (63 years old).
This study investigated the mechanisms that help to stabilize the head during head tilt in normal subjects and in patients with absent labyrinthine function. Seven normal subjects and four patients were examined. They were seated in a gimbal with limbs and torso restrained and head free to move. The gimbal could be tilted from upright to pitch or roll about earth horizontal axes. Tilt stimuli were delivered under two conditions: i) while performing mental arithmetic with eyes closed. ii) while reading fixed N six test type. During tilt, position and acceleration of the trunk and head and neck EMGs were recorded simultaneously. Initial responses was similar for all subjects; following gimbal tilt, the had tended to lag behind the trunk because of intertial lag.. After that, movement of the head on the trunk varied widely with three broad types. i) Head held relatively fixed to trunk. This tactic was deployed by normal subjects and one patient. ii) Unstable head on trunk. This response was typical of patients with labyrinthine defect. iii) Effective compensatory head movement. Only normal subjects had effective compensatory movement. Regarding head stability in space, all subjects had superior stability during reading than mental arithmetic. All patients had significantly poorer stability than normal subjects during pitch tilt backwards. The stability of the two patients tested in roll tilt was at the upper limit of the normal range. The latency of the initial large burst of EMG varied depended on the mean rate of change in head acceleration (jolt). The pattern of the latency in proportion to jolt did not show a clear difference between normal subjects and patients. These results suggest that the short bursting of the neck muscles during sudden tilts is non-stretch and non-vestibular in origin and other candidates for the origin could exist.
The nucleus of the optic tract (NOT) serves as an important visuo-motor relay between the retina and preoculomotor structures that mediate horizontal optokinetic nystagmus. In the present study, projections from the NOT in the brainstem were investigated using anterograde and retrograde tracers. Following biocytin injections into NOT, labeled fibers were observed in each of the following efferent pathways: 1) those that project to the contralateral NOT via the posterior commissure; 2) those that course through the nucleus reticularis pontis oralis to terminate the nucleus reticularis tegmenti pontis; and 3) those that descend via the medial lemniscus to the level of the medulla to terminate in the dorsolateral pontine nucleus, nucleus prepositus hypoglossi, descending and medial vestibular nucleus and the dorsal cap of the inferior olive. The projection from the NOT to the vestibula nuclei were demonstrated following WGA-HRP injections into the vestibular nuclei. Direct projections from the NOT to the descending and medial vestibular nuclei may contribute to the residual optokinetic responses of the vestibular nuclei neurons following cerebellar or inferior olivary lesions.
This study investigated the visual-vestibuloocular reflex in patients with vestibular disorders. Head and eye movements during active horizontal head oscillations were recorded using apparatus for examining the vestibuloocular system. Transfer function of the oculomotor system was calculated using head movement as the input and eye movement as the output. The examination was performed under the following 2 conditions: a) visual fixation on a fixed target in a lighted room (test for visual-vestibuloocular reflex, VVOR), and b) image fixation on a fixed target in the dark (test for vestibuloocular reflex, VOR). The data obtained were compared with previously reported reference intervals. Two patients with bilateral vestibular disorders and fifteen patients with unilateral vestibular disorders were examined. Results 1) bilateral vestibular disorders: On VVOR test, the breakpoint frequencies of the gain were lower than the reference intervals. On VOR test, the gains at 0.1 Hz were lower than the reference intervals, the slopes of the gain enhancement were not linear. 2) unilateral vestibular disorders: On VVOR test, the breakpoint frequencies of the gain were lower than the reference intervals in 75% of patients that were examined within two months after onset, 55% of patients that were examined two or more months after onset. On VOR test, the gains at 0.1 Hz were lower than the reference intervals in 75% of patients examined within two months, and in 64% of those examined after two or more months, the slopes of the gain enhancement were not linear in 100% of patients examined within two months, and in 73% of those examined after two or more months.
We examined the origin of regenerated hair cell, triggers for regeneration and cell death in the avian basilar papilla and the possibility of hair cell regeneration in the mammalian vestibular sensory epithelia. 1) To determine the origin of regenerated hair cells, we did an immune-TEM study using bromodeoxyuridine (BrdU) in damaged basilar papilla after noise exposure. Label-ing in the basilar papilla was initially detected in the supporting cells, which suggested that supporting cells were the original cells of regenerated hair cells. We examined two candidates of triggers for regeneration in damaged basilar papilla using an organ culture technique. One of the candidates was epidermal growth factor (EGF) and another was the extrusion of hair cells. Regarding the extrusion of hair cells, we compared those after collagenase treatment with those after noise exposure. Consequently, EGF had a potency to stimulate cell proliferation. Cell proliferation was recognized after noise exposure but not recognized after collagenase treatment. These results suggested that EGF might be one of triggers but extrusion itself could not be a trigger. 2) We examined whether apoptosis occurred during the process of hair cell regeneration after noise exposure using the TUNEL method. Consequently, apoptosis was recognized in hair cells just after noise exposure and at 2 days after noise exposure, which suggested that hair cell damage induced by noise exposure was due to apoptosis and apoptosis took part in the process of hair cell regeneration. 3) We did an in vivo immunohistochemical study using BrdU in the ampullar cristae after damage by gentamicin in the guinea pig. Labeled cells were recognized in the luminal portion of the sensory epithelia 60 days after gentamicin treatment, which indicated a possibility of hair cell regeneration in the vestibular epithelia.