The vestibular sympathetic fibers were examined in 20 guinea pigs by the immunohistochemical demonstration of tyrosine hydroxyrase and dopamine β-hydroxylase. The vestibular sympathetics originated in the ipsilateral superior cervical ganglion and entered the internal auditory canal along the labyrinthine artery. At the Schwann-glial border, some of the sympathetic fibers left the artery and went into the superior and inferior division of the vestibular nerve and made a loose meshwork among the Scarpa's ganglion cells while other fibers kept following the labyrinthine artery. Both groups of fibers entered the crista ampularis and saccular and utricular maculas after several bifurcations in the cribrose areas and terminated either near the capillaries beneath the sensory epithelia or among the vestibular nerve fibers. Some sympathetic fibers made direct contacts with the vestibular efferent fibers or the vestibular afferent fibers at the node of Ranvier. Sympathetic fibers were not observed in the sensory epithelia or semicircular canals, and were rarely found in the vicinity of the dark cells. The vestibular nucleus was also innervated by another catecholaminergic nerve fibers, which originated from the locus ceruleus, and the synaptic contacts were observed between the catecholaminergic nerve terminals and other neurons. These two peripheral and central catecholaminergic nervous systems were quite independent at the level of Schwann- glial border. Similar distribution of the sympathetic fibers were observed in the cochlea and the endolym- phatic sac also showed sympathetic nerve supply.

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Although the neural organization of the vestibular nucleus has been analyzed in detail recently, there have been few systematic studies of possible excitatory neurotransmitters of these neurons. Glutamate is thought to be one of the excitatory transmitters in the nucleus. It has been reported that NC 1200 is one of the most potent blockers of glutamate, and that the mechanism of action of the chemicals appears to be blocking of the alutamate channel. The present study was designed to explore the effects of NC 1200 on the vestibulo-ocular reflex. Eye movements of cats during horizontal rotation were recorded by the search coil method. NC 1200 was applied in 3mg/kg steps, to 12mg/kg. Numbers and amplitudes of nystagmus and velocities of slow and fast phases of nystagmus were measured before and after administration of NC 1200. Inhibition of the slow phase velocity was produced by a relatively low dose (3mg/kg), but the action against the fast phase velocity was produced only by a high dose (9mg/kg). The amplitude of nystagmus was suppressed by a high dose (12mg/kg).

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The relationship between the vomiting center in the medulla oblongata by Wang and the vestibular nucleus still remains in obscure. In order to investigate the central mechanism of the vomiting caused by vestibular stimulation, the intragastric pressure, gastric peristalsis and respiration during electric stimulation on the medullary vomiting center and on the semicircular canal nerve were recorded in 7 adult cats.
Movement of the stomach and respiration were recorded by change of the intragastric pressure in a baloon-transducer system and by change of the thoracic size, respectively, in the anesthetized cat.
The stimulation of the brain stem induced marked decrease of intragastric pressure in all cats and suppression of the peristalsis in 4, but suppression or excitation in respiration depending on the condition of anesthesia and the mode of stimulation was observed. Suppression of the gastric movement by canal nerve stimulaion was observed in only one cat. The position of the tip of electrode at the lateral border of the reticular formation of the medulla oblongata was confirmed histologically in each animal.

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Using urethane-chloralose anesthetized and artificially ventilated rats, the effect of vestibular stimulation on cerebral blood flow (CBF) was investigated. CBF in the parietal cortex was measured continuously by laser Doppler flowmetry. Caloric vestibular stimulation with cold water (0°C) produced decreases of both systemic blood pressure (BP) and CBF. Electrical stimulation of vestibular nerve was performed by placing the electrode on vestibular and cochlear window. Electrical vestibular stimulation also produced decreases of BP and CBF which are intensity-dependent. In addition, chemical (L-glutamate) activation of vestibular nucleus produced a similar effect. Following spinal transection at the first thoracic level, both BP and CBF responses by electrical vestibular stimulation were abolished. It was concluded that vestibular stimulation produces a decrease in CBF and it appears to be a secondary effect of depressor response.

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In order to clarify the relation between motion sickness and vestibulo-aotonomic nerve responses, we recorded heart rate (HR) and coefficient of variation of R-R interval (CV-RR) in seven rabbits and ten young men before, during and after linear oscillations stimulation frequency 0.29 Hz and amplitude 50 cm for 300 or 360 sec. Only stimulation of X direction made large body responses in the rabbit, namely, HR decreased and CV-RR increased. And after atropine injection or bilateral labyrinthectomy, these responses vanished. These results suggested that vestibulo-parasympathetic nerve reflex played an important role in these responses. As for the human, autonomic nerve responses were unstable before and during linear oscillatory stimulation for the subjects who had susceptibility of motion sickness.

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The characteristic of cervicovestubular syndrome is paroxysmal vertigo provoked by the turning of the cervix. For many patients with this syndrome, the authors performed the perivascular sympathectomy of “the affected side vertebral artety” and noticed remarkable effects for paroxysmal vertigo. From the results of operation, it was suggested that the origin of vertigo would be the abnormal irritation of the perivascular sympathetic nerveplexus caused by the cervical turning. This sympathetic fibers originate in the ipsilateral superior cervical ganglion. So the experimental results which stimulated the superior cervical gangion of guinea pigs were discussed.

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Stress is an important factor in the occurrence of vertigo. In this experiment, we have shown that the noradrenergic neurons of the locus coeruleus (LC), which is known as the central sympathetic nervous system, reveal axonal sprouting or degeneration in response to chronic stress. The density of noradrenergic LC fibers in the rat cerebral cortex was quantified using antidromic stimulation technique. We introduced “P-index”(projection index), which is defined as the percent of LC neurons showing antidromic response to cortical stimulation taking the total number of LC neurons recorded as 100. The P-index was significantly higer in animals which had received repeated mild stress, but lower after relatively severe stress. Thus, axonal sprouting of LC neurons may occur following mild stress, whereas severe stress may cause axonal degeneration. Since sympathetic noradrenergic neurons resemble LC neurons in most properties, plastic changes similar to those occurring in LC neurons may occur in the sympathetic nerve. If this is the case the pathology of vertigo may involve the axonal sprouting or degeneration of sympathetic noradrenergic neurons.

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Autonomic nervous system controls cardiovasucular system. And its disturbance may alter general circulatory condition. On the other hand, it has been believed that inner ear blood flow is deeply related to inner ear diseases such as Meniere's disease or sudden deafness. Therefore in this study vasoactive agents (dobutamine, angiotensin II and dilazep dihydrochloride) were injected intravenously to guinea pigs and change in inner ear blood flow was measured by laser Doppler flowmetry. Because of anatomical difficulty in measuring vestibular blood flow, cochlear blood flow was monitored.
Dobutamine increased blood pressure, cochlear and cutaneous blood flow. Angiotensin II also elevated blood pressure and cochlear blood flow and decreased cutaneous blood flow. Meanwhile dilazep decreased blood pressure and cutaneous blood flow, but characteristically increased cochlear blood flow.
In addition, lethal dose of pentobarbital was injected, and then cochlear blood flow seemed to be resistant to fall of blood pressure.
On the basis of these results there seems to exist some autoregulatory system to preserve cochlea blood flow. Blood supplies to vestibular organs are the same as those to cochlea, or ginating from the verte- brobasilar artery. Therefore vestibular blood flow may possibly react in the same way as cochlear blood flow does.

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We examined autonomic nervous function and cerebral blood flow in 17 patients with vertigo and dysequilibrium. In the 17 patients, 13 showed positive and 4 negative in the Schellong test. We measured ECG RR interval change between supine and standing positions.
In the cerebral autoregulation test using single photon emission CT (SPECT), subjects were judged to be positive if their blood flow in standing position dropped 10% or more from that in supine position. The results obtained as follows. 1) Autonomic nervous system dysfunction does not influence cerebral autoregulation. 2) Dizziness when assuming a standing position seems to be associated with autonomic nervous dysfunction. 3) We also surmised that the autonomic dysfunctions might have some relationship to the low vestibular blood flow which is undetectable by SPECT alone.

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In order to clarify the participation of the autonomic nervous system in vertigo and pseudovertigo, clinical and experimental studies were carried out from the cerebral circulatory point of view.
Thirty-three patients with brainstem or cerebellar stroke and 48 age-matched healthy volunteers were subjected to the functional tests of autonomic nervous system. The patients with vertigo or pseudovertigo showed a significant hyporeactivity to Aschner's eyeball pressure test, and significant hyperresponses or distinct differences between lesion and non-lesion sides to both carotid sinus massage and cold pressor tests.
Vasomotor responses of the vertebrobasilar system and carotid arterial system were compared in 33 monkeys. The vasomotor responses to changes in blood pressure were significantly lower in the former than the latter. Contrastly, the vasomotor responses to changes in PaCO₂ were higher in the former.
In conclusion, the autonomic dysfunctions and altered vasomotor responses in the vertebroasilar system could play an important role in the emergence of vertigo or pseudovertigo.

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The auditory pupillary responses of both eyes were analysed in 15 normal subjects using a computed pupillograph. A pupillary dilatation was obtained after unilateral auditory stimulation in all cases. Four cases showed monophasic pupillary dilatation, while 11cases showed biphasic pupillary dilatation. The latency time of dilatations was 400-570msec. Both eyes showed same type of responses. Two drops of 10% guanethidine, sympathetic blocking agent, were applied on one eye showing biphasic pupillary dilatation. Although the first phase was little affected, the second phase was obviously inhibited. This may explain that the first phase is caused by the inhibition of parasympathetic nervous system and the second phase by the excitation of sympathetic nervous system. We intend to apply the auditory pupillary responses for the examination of autonomic dysfunction in patients with Meniere's disease.

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To assess the autonomic function of the patients of vertigo, we measured the sensitivity of baroreflex using norepinephrine, to produce the increase of bloodpressure and trinitroglycerin, to produce the decrease of blood pressure. As a result, in the patients of vertigo, parasympathetic nerve activity was hypofunction whatever site they were involved.
In the patients of Meniere's disease, at the time around the attack, at the time near the onset of the disease, at the time of active state of the disease, synpathetic nerve activity was hyperfunction. And positiveness of Schellong's test was thought to be related to the hyperactivity of the baroreflex.
On the other hand, spectral analysis of R-R interval revealed that in the patients of Meniere's disease, the parasynpathetic nerve activity tend to be hypofunction.

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To clarify the autonomic nervous function of vertiginous patients, heart rate variation on deep breathing (correspond to parasympathetic function) and on standing (correspond to sympathetic function) were measured by Autocorder HR200 (Japan Medics Co Ltd).
The subjects were consisted of 61 patients with Meniere's disease (130 cases), 21 patients with vestibular type of Meniere's disease (28 cases), 51 patients of unknown origine (64 cases) et al, and total were 207 vertiginous patients (309 cases).
In many vertiginous patients including Meniere's disease, parasympathetic function was decreased.
Sympathetic function was also decreased in Meniere's disease, and its function was elevated and revealed sympathetic predominant state at attack stage. Concerning above mentioned autonomic abnor- mality, we speculated that decreased parasympathetic function was important and change of sympathetic function was secondary.

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