To see whether hypertension of the cervical soft tissues participates in producing vertigo due to whiplash injury, we developed two types of equilibrium tests: equilibrium tests with anodic low-frequency pulse stimulation of the neck and equilibrium tests after fixing the neck with a collar. Disequilibrium due to whiplash injury was often aggravated by pulse stimulation, whereas it tended to decrease or disappear on fixing the neck with a collar. These findings indicate that hypertension of the cervical soft tissues is often an important factor in the development of vertigo due to whiplash injury. To investigate the possible existence of hypothalamo-brain stem dysfunction in vertigo cases with whiplash injury, we carried out equilibrium tests with adrenaline loading. These tests showed that in most cases with vertigo, ataxia appeared or was intensified by adrenaline loading. We concluded that hypothalamo-brain stem dysfunction is a possible etiologic factor in the development of vertigo due to whiplash injury. From these observations it seemed that vertigo due to whiplash injury develops because abnormal centripetal impulses arising from the injured cervical soft tissues reach the hypothalamo-brain stem cause manifestation of dysfunction in these parts of the brain. Thus, marked ataxia of the eyes and body might result, which would lead to vertigo in these cases. Therefore, treatment for this kind of vertigo should be directed to improve impaired function both (i) in the cervical region and (ii) in the hypothalamo-brain stem system.
Four cases with similar symptoms of fits consisting of vertigo, headache, disturbance of consciousness, and spasm, are presented. Two of them were confirmed by operation to have haemoatoma in vermis of cerebellum. 1) "The acute vermis syndrome", is defined and characterized in order to facilitate diagnosis in the future. 2) The characteristic nystagmus observed in these cases, are named "the irregular burst of spontaneous horizontal nystagmus". It is presumed that said nystagmus might be caused by disturbance in an intermediate part of vermis of cerebellum, particularly fastigial nuclei of both sides. 3) It is presumed that "vertical positioning nystagmus with vertigeous sensation" seen in the four cases might be caused by lack of vestibular repression due to the disturbance in the lower vermis.
A 4-channel radio-telemeter, capable of transmitting eye and 3-dimensional head movements, was devised and eye and head movements in ballet rotation were observed. The purpose of this study was to observe the mode of appearance of nystagmus during intentional movements, and to elucidate the role played by vestibulo-ocular reflexes in intentional movements. 1. In observations of "tours chaînés" the appearance of one-beat nystagmus per rotation was recognized. This kind of nystagmus was produced by ballet dancers intentionally by means of jerking movements of the eye and head, i.e., spotting. The multiple irregular perrotatory nystagmus appearing during passive rotation was suppressed in ballet rotation by intentional spotting technique. That is, the will controlled reflexes. 2. In the record of beginners' "tours chaines, " multiple irregular nystagmus was recognized. That is to say, the ability to intentionally control perrotatory nystagmus appearing reflexly was acquired through training. 3. The one-beat-per-rotation nystagmus appearing in ballet rotation. was analyzed in terms of head movements in "pirouette rotation". As a result it wast found, that this intentional eye movement was a motion to coordinate with the vestibulo-ocular reflexes provoked by jerking head movements such as spotting. In other words, intentional movements were carried out by the use of reflexes. 4. Postrotatory nystagmus in "fouette en tournant" was observed. When the eyes were kept open after rotation, postrotatory nystagmus was not observed, but when the eyes were closed after rotation, active nystagmus appeared. The suppression of postrotatory nystagmus in ballet rotation is largely due to visual fixation.
Experiments were performed on chloralose anesthetized cats to analyze longitudinal vestibulo-spinal coordinations. Stimulation of vestibular afferent nerves elicited two reflex responses from bilateral spinal outflows, early and late, from spinal ventral and dorsal roots and cord dorsum. The early part of the spinal response may be due to the relatively direct bypasses the bulbar reticular formation. In contrast the bulbar reticular formation may be underlying the late part of the spinal responses. Alternately, asphyxia and Nembutal anesthesia affected the late part of spinal responses more easy to abolished than the early ones. Prolonged blocking interaction was obtained between the late part of the vestibular evoked spinal responses and other reflex responses, i.e., spino-bulbo-spinal, spino-bulbo-cranial and cortically evoked extrapyramidal activities.These reflexes were relaying the bulbar reticular formation, thus, these blocking may be obtained at the bulbar level.
Effects of cervical dorsal root and sympathetic stimulations on the vestibular motoneurons responses recorded from the radial nerve of the cat were analysed to calrify etiological factors involved in vertigo caused by whiplash injury. The late activities of the vestibular response were attenuated during repetitive stimulation of the cervical sympathetic nerve. These activities were also inhibited by cervical dorsal root stimulation. No effect was seen in the initial spike of the vestibular response during such modulating stimulation. However, the inhibitory effect of sympathetic stimulation on the initial spikes was detected when the recovery curve of the initial spike during sympathetic stimulation was compared with that during a no stimulation period. This comparison of the two recovery curves also revealed inhibitory effects on the late activities. Based on these results, some etiological factors in vertigo as a sequelae of whiplash injury were discussed.
In vivo morphological observations of the semicircular canals have been seldom reported because they lie deep within the temporal bone. The author excised the semicircular ampullae of frogs in Ringer's solution, resected the top of each semicircular ampullae to make a round hole, and observed the inside with a dissection microscope and a scanning electron microscope (SEM) as well as a light microscope.
We have investigated and discussed the possible mechanisms of dizziness or vertigo due to involvement of the cervical sympathetic system with data obtained by stimulating the stellate ganglion and the vertebral nerve or plexus in a series of 15 patients during surgical treatment of episodic vertigo (Powers' syndrome)12. Some of the neural pathways and the mechanisms of cervical vertigo due to disorders of the cervical sympathetic system are postulated. The data obtained is summarized as follows: 1) Stimulation of the periarterial nerve produced manifold varieties of pupillary changes with or without ocular movements, nystagmus and subjective symptoms; the pupillary changes included slow and mild mydriasis or miosis either on the ipsilateral or contralateral pupil and the hippus. Ocular movements, nystagmus and subjective symptoms observed in only some of the cases included conjugate or disconjugate eye movements, horizontal and vertical nystagmus, and occipito-cervical dull ache and dizziness. 2) Stimulation of the stellate ganglion produced prompt and full mydriasis of ipsilateral pupil without any subjective symptom, coular movement or nystagmus. From the data available, it seems likely that: 3) Periarterial nerve structure including the vertebral nerve and plexus (which had been called the "deep or posterior cervical sympathetic system" by French investigators) is functionally or physiologically different from the cervical sympathetic system, including the inferior sympathetic or the stellate ganglion (which had been called the "anterior cervical sympathetic system" by French investigators). 4) The stellate ganglion proper has little significance in a development of the cervical vertigo.
The optic vestibular coordination, by utilizing the optokinetic and labyrinthine stimulations, was investigated in the squirrel monkey subjects. Simultaneous labyrinthine stimulation (subliminal) facilitated the slow phase eye-speed of optokinetic nystagmus. The optokinetic adaptation limit was elevated, in this instance, and the speed of retinal nystagmus was improved. In other words, the presence of simultaneous vestibular stimulation possibly stabilized the retinal image of a faster moving target. Therefore, the concept; the vestibular system has a physiological role in assisting the stabilization of retinal image, was confirmed. The methamphetamine administration also facilitated the slow phase eye-speed of optokinetic nystagmus.
In order to clarify racial variation in the occurrence and manifestation of Meniere's disease, 545 "dizzy patients" including Japanese, American Whites, and Negroes were examined. The results obtained were as follows: 1) The incidence of Meniere's disease was not extremely lower among the American Negroes than among the Whites. 2) The duration of the disease was longer and vertiginous attacks were more frequent among American Whites than among Japanese subjects. 3) The incidence of accessory symptoms such as nausea, vomitting, and headache was almost the same for American Whites as it was for Japanese subjects. The spontaneous manifestations of equilibrium seemed to be more disturbed in American Whites than in Japanese subjects. The variations in the manifestation of Meniere's disease among races was assumed to be due not only to heredity but also, strongly to environmental differences.