Isao Kato

Role of the nucleus of the optic tract in monkeys in relation to optokinetic nystagmus

Nine monkeys were used in order to clarify the role of the nucleus of the optic tract (NOT) in the generation of optokinetic nystagmus (OKN). In 3 monkeys whose NOTs were almost totally damaged, optokinetic stimulus toward the lesioned side failed to generate either eye deviation or OKN and revealed only voluntary saccades, whereas that toward the side contralateral to the lesion generated normal gain of OKN. The phenomenon was identical in either monocular or binocular stimulation. In two of 3 monkeys whose NOTs were partially destroyed, optokinetic stimulus toward the lesioned side produced OKN, but the gain of OKN, but the gain of OKN was at maximum less than 60% in both binocular and monocular stimulation. In the remaining one monkey whose NOT was injured, but superficially, OKN showed normal gain in both directions. In 3 other monkeys whose NOTs were spared, this OKN asymmetry was not observed. Pursuit and saccadic eye movements were normal in all NOT-lesioned monkeys. Visually induced eye movements in the vertical axis were likewise normal. The present experiment suggests that the NOT in monkeys may be the first relay station in the horizontal optokinetic path and that in primates as in non-primates both crossed and uncrossed fibers reach motor centers for OKN via the NOT.

Loss of Visual Suppression of Caloric Nystagmus in Cats

Loss of visual suppression (VS) of caloric nystagmus was produced after creating flocculus lesions. The flocculus receives visual signals through a climbing fiber pathway via the inferior olive (IO) and through a mossy fiber pathway (MF) presumably via the superior colliculus (SC). In order to elucidate the prefloccular nuclei responsible for VS of caloric nystagmus, VS of caloric nystagmus was investigated after making lesions in such nuclei as the SC and the IO in 42 cats. After the IO lesion, VS of caloric nystagmus was revealed in all IO-lesioned cats throughout the whole experimental course. After the SC lesion, loss of VS was constantly observed and persisted in 7 out of 9 cats. Hence, the MF pathway via the SC is believed to be the most likely candidate for the immediate modification of the vestibuloocular reflex by visual stimuli.

Role of the nucleus reticularis tegmenti pontis on visually induced eye movements

Abstract Optokinetic nystagmus (OKN) and visual suppression of caloric nystagmus were tested in cats with electrolytic lesions in the nucleus reticularis tegmenti pontis (NRT) or with hemicerebellectomies. The animals with a NRT lesion could follow higher stimulus velocities, but the eye movement output saturated at 10°/s. In the hemicerebellectomized cats, on the other hand, slow-phase OKN velocity was normal at stimulus velocities less than 30°/s. In addition, OKN impairment was more transient in the cats with hemicerebellectomies than in those with NRT lesions. In the cats with a NRT lesion, loss of visual suppression of caloric nystagmus was apparent in nystagmus with the slow phase toward the lesion side, whereas in cats with hemicerebellectomies, it was toward the contralateral side to the lesion. These findings suggest that the NRT may be a part of the relay nuclei mediating optokinetic signals responsible for OKN at all optokinetic stimulus velocities and the flocculus may be responsible for OKN at higher optokinetic stimulus velocities. In addition, the NRT may also be one of the prefloccular nuclei conveying visual input signals responsible for visual suppression of caloric nystagmus to the contralateral flocculus.

Temporal Bone Findings in a Case of Sudden Deafness and Relapsing Poychondritis

Light microscopic examination was made of the right temporal bone from a 57-year-old female who developed sudden total hearing loss in both ears 1 year before death. The patient had suffered from relapsing polychondritis for 1 1/2 years prior to death. Pathological changes were compatible with known viral endolymphatic labyrinthritis. Slight ossification and fibrous tissue proliferation in the perilymphatic space seem to have been caused by a spread of infection from the middle ear. Susceptibility to viral infection in the labyrinth in patients with a long-devastating illness is discussed.

Caloric Pattern Test with Special Reference to Failure of Fixation-Suppression

Fixation-suppression of caloric nystagmus was studied in 1230 consecutive cases. An analysis of caloric nystagmus with failure of fixation-suppression (FFS) made it possible to classify patterns of FFS into three types: Type I: FFS was observed bilaterally in caloric nystagmus; Type II: FFS was recognized unilaterally on either side; Type III: FFS was seen in either direction of nystagmus. On the basis of these three types, the underlying neuroanatomical substrate responsible for FFS is discussed.

The Fast-phase Velocity of Optokinetic Nystagmus in Central Nervous System Disorders

The fast phase of optokinetic nystagmus (OKN) in patients with central nervous system (CNS) disorders was quantitatively evaluated using a micro-computer. The relationship between peak velocity of the fast phases of OKN (velocity(p] versus amplitude was recognized to be best fitted to an exponential equation, i.e., velocity(p) = K(1-exp[-amplitude/L]). In patients with lesions in thalamus, midbrain, or pons, the velocity(p) was significantly reduced, whereas in patients with lesions in the medulla or the cerebellum, it was normal. The directional asymmetry of velocity(p) toward the lesion side indicated that the velocity(p) toward the intact side was significantly reduced as compared with that toward the lesion side in patients with lesions in the thalamus or midbrain, whereas in patients with lesions in the pons, the velocity(p) toward the lesion side had decreased significantly as compared with that toward the intact side. Thus the quantitative evaluation of velocity(p) may provide some important information on the mapping of lesions in patients with CNS disorders.

Visual suppression of caloric nystagmus in cats.

A newly devised animal box with which caloric tests can be easily performed in the awake cat is presented. This device is also useful for position and optokinetic tests. Visual suppression of caloric nystagmus was investigated in such vertebrates as monkeys, cats and rabbits. There was a definite species difference in the rate of visual suppression of caloric nystagmus. It may be that the difference among species is due to a difference in fixation function among animal species.

Visual Suppression of Caloric Nystagmus and Optokinetic Responses in Cats

Previously it was reported that loss of visual suppression (VS) was accompanied by disturbance of optokinetic nystagmus (OKN) in monkeys with lesions at the flocculus. In the present experiment with cats, OKN was investigated after inflicting lesions on either superior colliculus (SC) or inferior olive (IO), both of which are considered to be the main prefloccular relay nuclei to mediate visual signals to the flocculus. VS of caloric nystagmus was recognized in all the IO-lesioned cats and OKN remained normal except in one cat. After the left SC lesions, loss of VS was evidently revealed and optokinetic stimuli produced directional preponderance to the left with diminished responses to the right in 7 of 9 cats. The present findings suggest that the SC may be an important relay nucleus to the flocculus in conveying visual signals responsible for VOR gain.

Visual Fixation of Caloric Nystagmus with Special Reference to a New Index

The effects of visual fixation upon caloric nystagmus were computed in each parameter as a measure. The percentage reduction established with slow-phase velocity best distinguished normal from abnormal visual fixation at the line of 60%. However, if a +/- 5% safety margin is taken into account, 11 of 176 ears showed false-negatives. The number of nystagmus beats in normals decreased markedly during the period of fixation. In abnormals, the number of nystagmus beats increased definitely during the fixation period. Based on this fact, the product of slow-phase velocity multiplied by the number of nystagmus beats was assessed as the fixation-suppression index. As a result, 11 ears showing false-negative slow-phase velocity decreased to 2 ears. Thus, this modified fixation-suppression index seems to be an appropriate parameter to separate normal from abnormal fixation-suppression of caloric nystagmus.

Electrooculographic evaluation of methylmercury intoxication in monkeys

Abstract Methylmercury chloride (MeHg) was administered to five monkeys. Electrooculography (EOG) was used as an objective measure of vestibular and oculomotor functions. Monkeys with acute and subacute exposures to MeHg exhibited spontaneous nystagmus and positional nystagmus of the apogeotropic type which were the earliest indications of dysfunction prior to the onset of clinical signs and symptoms. In these monkeys the slow-phase velocity of optokinetic nystagmus (OKN) waxed and waned with every test. At velocities of optokinetic stimuli greater than 50°/s, the slow-phase velocity of OKN fluctuated during every test and lagged behind the velocity of the optokinetic stimuli. The second and third phases of optokinetic after-nystagmus appeared at an early stage of the experiment, and were accompanied by the second and third phases of caloric nystagmus. Visual suppression (VS) of caloric nystagmus was normal for MeHg dosages up to 10 mg/kg. Larger dosages resulted in a loss of VS which was observed several days before severe neurological signs and symptoms appeared, and OKN was impaired. Monkeys which were administered minimum MeHg dosage equal to one-tenth of those in monkeys with acute and subacute exposures did not show any neurological or histological changes. The only significant positive signs were spontaneous nystagmus and positional nystagmus. Hence, the EOG is very sensitive to functional disturbances and can be utilized to detect dysfunction in MeHg intoxication.