The fine structure of human vestibular ganglion cells was studied in serial sections under the electron microscope. Most of these cells were unmyelinated and bipolar but a few were myelinated. Two types of unmyelinated multipolar cells were also observed, one large, similar in size to the bipolar cells, and the other smaller. Nerve fiber synapses were found among the small multipolar cells. One of these terminals contained mostly nongranular, spherical vesicles, and was primarily located on dendrites. The other contained many nongranular and granular ellipsoidal vesicles and was found in the perikaryon or the dendrites. Whether these terminals are of the same or different origins is yet to be determined. However, the existence of multipolar cells and synapses among these cells correlates with the reports on the neurophysiology of interreceptor and efferent activities in the vestibular nerve system. Another consideration is the dual autonomic innervation of the vestibular ganglion cells based on the presence of two types of nerve terminals.
The vestibular apparatus in human fetuses and adults was examined by scanning electron microscope. 1. The intermingled coexistence of immature and mature sensory cells over the sensory epithelium of the vestibular organs was seen in specimens from 14 to 18-week-old fetuses. The number of stereocilia in each sensory hair bundle was almost the same in the immature and mature cells. Thus, small fetal stereocilia seem to grow into mature long hairs. 2. Smallsensory cell groups were found apart from the maculae and cristae in one fetal and one adult vestibule. Both groups were seen in the utricular wall, one near the utricular macula and another near the posterior ampullary crista. Such crista neglect-like structures seem to occur sometimes in the human vestibule. 3. Non-sensory ciliated cell groups were found in seven fetuses aged 14 to 25 weeks. These cells were scattered in boundary areas between the three semicircular canal ampullae and the utricle. As these cells were not found in adult specimens, it seems likely that they disappear during maturation.
The thalamo-cortical relay neurons (TCR) of the nucleus ventralis lateralis of the cat's thalamus were examined after the intracellular injection of horseradish peroxidase, and 20 TCR neurons were reconstructed three dimensionally. (1) TCR neurons are medium or large spheroidal cells. The dendritic field is about 380630μm, and the diameter of the cell bodies is about 2050μm. The cells have 48 principal dendrites and the dendrites arborize near the cell bodies. Finally the branches terminate in 73-148 terminal knobs. All dendrites have many spines except in their initial parts. (2) The axons of TCR neurons originate from the cell bodies and run antero-laterally, pass through the reticular nucleus of the thalamus, and enter the internal capsule. The axon collaterals are observed within the reticular nucleus of the thalamus. It seems that these collaterals are involved in recurrent collateral inhibition. (3) The axons of TCR neurons begin to branch in the white matter just below the gray matter of the motor cortex, and several branches enter the gray matter. In the gray matter the branches bifurcate several times and finally terminate mainly in the third cortical layer, and also some in the first layer. The projection area of the axons of single TCR neuron in the motor cortex is more than 2.0mm×2.0mm
The anatomy of the vestibular aqueduct (VA) and rugose potion (RP) of the endolymphatic sac (ES) was examined. Serial horizontal sections of 79 normal temporal bones of individuals aged 20 to 102 yeras were used. Medial view graphic reconstruction of the VA was performed for each specimen in order to determine the area, length, and location of the VA. The relationship between the width of the VA and the area of the VA, and the relationship between the degree of development of the VA and the degree of development of the temporal bone (periaqueductal pneumatization and the otic capsule in the periaqueductal region) were also investigated. In addition, measurements of the RP were made, further histo-logical study of the RP was performed in 30 selected specimens. We found that 1) the VA in adult temporal bones varies in size and can be classified as hypoplastic, normoplastic, or hyperplastic; 2) many of the VAs in each group mentioned above have similar sizes, although they vary in length, angle, or location; 3) all or most of the RP was located within the VA in all but one specimen, which had a hypoplastic VA; 4) the histology of the RP was characteristic in each type of VA; 5) the degree of development of the VA seems to correlate with the degree of development of the otic capsule in the periaqueductal region.
The neural connections of the cerebello-thalamocortical pathways of the cat were investigated electrophysiologically. Intracellular recording was performed from pyramidal tract neurons (PTNs) in the motor cortex and relay neurons in the ventrolateral nucleus of the thalamus (VL). Stimulation of the separate cerebellar nuclei, the interpositus nucleus (INP) and the dentate nucleus (DN), evoked EPSPs with latencies of about 3msec in the fast PTNs. With stimulation of the separate nuclei and intracellular mapping of evoked EPSPs in the motor cortex, it was found that there were many PTNs that receive convergent inputs from INP and DN in the whole area of the motor cortex. Since it is known that the cerebello-thalamo cortical pathway to fast PTNs is disynaptic, the next question was where the convergence of the inputs from both cerebellar nuclei occurred, at the level of the motor corrtex or the VL. By combined stimulation of both nuclei at various intensities, spatial facilitation and occlusion of evoked EPSPs were observed in fast PTNs. This result suggests that the convergence occurred at the level of the VL. In order to demonstrate this convergence of the inputs from both nuclei in the VL, we performed intracellular recordings from VL relay neurons. Large unitary EPSPs were monosynaptically evoked in a single VL relay neuron after stimulating DN as well as INP. It was concluded that the convergence of the inputs from INP and DN occurs at least partly in the thalamo-cortical neurons of the VL.
Stimulation delivered to the mesencephalic locomotor region (MLR) in the acute decerebrate cat elicits “controlled” locomotion on a moving treadmill. Stimulation to the dorsolateral part of the MLR elicits alternating rhythmic shifting of the weight between hindlimbs (stepping) on a still surface. Stimulation to the MLR increases postural muscle tone of the hindlimbs augenting reflex standing of a decerebrate cat. The changes in the discharge characteristics of 84 neurons in the lateral vestibular nucleus (VLD-neurons) were studied during these locomotor movements and postural changes. VLD-neurons were antidromically identified and extracellularly recorded by means of microelectrodes. EMGs of representative hindlimb muscles were recorded. During hindlimb stepping and postural changes, the forces exerted at the foot contacts of the hindlimbs were measured by means of force transducers. The results obtained from 84 VLD-neurons (conduction velocity : 93.1±17.8m/s, firing rate : 12.1±11.5spikes/s) are summarized as follows : 1) With shortening of the cycle time during locomotion, the majority of VLD-neurons (43/54) tended to discharge rhythmically in phase with bursting discharges of the triceps surae muscle. The rest of the VLD-neurons (11/54) maintained tonic discharges irrespective of the changes in cycle time. 2) During hindlimb stepping, some VLD-neurons (8/16) exhibited rhythmic bursting discharges slightly preceding the onset of force increase in the ipsilateral hindlimb. 3) Most VLD-neurons (17/18) increased their tonic firing rates during augmented reflex standing. All these results demonstrate that VLD-neurons play roles not only in the phase contral system but also in the power or postural tone control system both during locomotor movements and postural adjustments.
Observation and follow-up study of abnormal eye movements were carried out in seven cases of acute unilateral cerebellar vascular disease. All of them were males who had survived the vascular attacks and were diagnosed as having cerebellar infarction by computerized axial tomography and vertebral angiography except for one case of cerebellar bleeding. Either gaze or spontaneous nystagmus was observed in all seven cases within 20 days of the onset, and positional nystagmus appeared in four of them. Ocular dysmetria, disturbance of smooth pursuit eye movements and suppression of optokinetic nystagmus were frequently observed. Pathological nystagmus towards the intact side and over-shooting eye movements to the diseased side in asymmetrical ocular dysmetria may be useful diagnostic features. Recovery from disturbed optokinetic nystagmus was corfirmed by observations of increasing maximal eye velocity and the frequency of optokinetic nystagmus in two cases during a long course of about 200 days
A study was made of 173 patients admitted to the hospital immediately after head injury. 1. Fifty-three (30%) complained of vertigo. Of the 44 patients under 9 years of age less than 14%. complained of vertigo. 2. The incidence of vertigo depended on the site of the lesion. It occured in 50% of those with occipital injuries, in 40% of those with blows to the temple, and in 20% of those with injuries of the face or forehead. 3. Skull fractures were found in 49 patients, and nearly 29% of them complained of vertigo, although vertigo itself is not necessarily associated with skull fracture. 4. Vertigo developed almost immediately after the injury in 19 cases, in 21 within 3 days, in 7 after a week and in 6 in 2-4 weeks. 5. Symptoms disappeared in 23 cases within 1 week, 16 within 2-4 weeks and 8 within 1-3 months, but in 2 cases vertigo persisted for 6 months. 6. Sixteen patients with head injuries and vertigo were seen only by neurologists. 7. Spontaneous nystagmus was seen in 10% of the cases and gaze nystagmus in 33%. Positional nystagmus was seen in 84% and positioning nystagmus in 86%. 8. Hearing impairment was found in 33% and an abnormal caloric test in 44%. 9. Eye tracking test and optokinetic nystagmus were abnormal in 37%. These results suggest that the positional nystagmus test is most useful in quickly detecting abnormalities in patients with vertigo after head injuries, though the site of the lesion can be determined by positional nystagmus tests only. In addition this test can rule out vertigo of psychosomatic origin or malingering.
In 290 patients with vertigo and 71 normal subjects, caloric nystagmus of the right and left eye was recorded separately, and the velocity of nystagmus of each eye was compared by electronystagmography. 1) In 42% the patients and 30% of the normal subjects, the inward movement of caloric nystagmus of each eye was faster than the outward movement. This difference was greater near the end of the calorigram. 2) This difference of velocity of each eye appeared not to be related to spontaneous or positional nystagmus. 3) Of 25 subjects with spontaneous or positional nystagmus, 24 showed like convergence and only one had divergent nystagmus (near the end of caloric nystagmus one eye continued to have caloric nystagmus but the other changed to spontaneous nystagmus). These results indicate a difference of the velocity of caloric nystagmus between the right and left eyes, especially of inward movement.
In 21 patients with surgically proven acoustic neuromas, auditory brainstem responses (ABR) were recorded, and the diagnostic value of ABR for detecting acoustic neuromas was evaluated. The ABR criteria were (1) wave V latency, (2) the latency delay between waves I and V (I-Vd), (3) interaural wave V latency difference (IT5) Diagnosis was confirmed in 86%. IT5 and I-Vd were approximately proportional to the size of the tumor. Thees, false negative examinations may be encountered in cases of small acoustic neuromas.
Thirteen patients with migraine complicated by severe vertigo were analysed statistically. (1) Six patients had classic migraine and 7 had common migraine. (2) Nine were females and 4 were males. (3) The mean age of onset of migraine was 25.9 years. However, the first attack of vertigo occurred at a mean age of 45.2 years. Thus, vertigo seems to be a late complication of migraine. (4) In all 13 cases, vertigo was spontanous, episodic and recurrent. The duration of the vertiginous attack was less than one day in most cases (76.9%). The vertigo pattern was of the rotatory type in 8, all of whom also had cochlear symptoms (tinnitus and/or hearing impairment), of the floating type in 3 and of the scotodinic type in 2. (5) In many cases (69.2%) vertigo occurred during the migraine attack or as an aura. The occurrence of vertigo as an equivalent of the migraine attack was seen in 10 cases (76.9%). (6) In most of the cases (76.9%), vestibular function was normal during vertigo-free intervals. (7) Drug therapy was not very effective in many cases, but in 3 patients, all of whom had classic migraine, sublingual nitroglycerin at the oncet of vertigo was successful in aborting the attacks.
So-called alternating nystagmus (involuntary eye movements in alternating directions) has been reported to occur frequently in congenital nystagmus. Moreover, the differential diagnosis of congenital nystagmus is relatively easy because of its numerous characteristic features, e.g., accompanied often by inverse OKN, devoid of oscillating vision except in the latent form, tending to become pronounced with fixation and diminished on closing the eyes and being a lifelong phenominon. In describing acquired alternating nystagmus as oposed to the congenital variety, Kornhuber pointed out that it occurs in the presence of extreme vestibular hyperfunction resulting from cerebellar disorders associated with impairment of the roof of the fourth ventricle, or in cases of syringobulbia or multiple sclerosis. The patient presented here had transient alternating nystagmus, presumably due to a similar underlying disease. CT-Scan revealed an abnormality in the posterior fossa. This case is presented in the hope that accumulation of such cases of acquired illnesses will help elucidate the pathogenetic mechanism of congenital alternating nystagmus.
Eye movements in an 8-year-old with congenital oculomotor apraxia were recorded and analyzed. The predominant defects were increased latencies and decreased amplitudes of voluntary saccadic eye movements in the horizontal plane. Abnormalities of eye movement were greatest when the oculomotor task required motor volition. In this patient complete loss of the quick phase of vestibular nystagmus was elicited by cold caloric irrigation and a moderate defect in the initiation of the slow and quick phases of optokinetic nystagmus were also present. However, the slow phase of vestibular nystagmus was demonstrated by caloric test and pendular rotation test to be preserved. Eye and head movements began nearly synchronously. The saccade did not occur consistently even after the head began moving and instead, compensatory eye movement occurred as the patient moved his head toward the target. Overshooting head movements were frequently observed. CT scan of the brain revealed atrophy of the cerebellar vermis. Our findings indicate that the patterns of eye-head coordination in this patient depend upon the nature of the defect in the production of voluntary saccade. The main lesions are probably in the PPRF and cerebellar vermis. These two lesions are believed to be congenital associated disorders of hypogenesis of myelination.