[Case of malignant pharyngeal tumor presenting as Garcin's syndrome].
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Biomedical subjects
Publications and source records attributed to E Sakata.
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During the examination of patients who complain of vertigo or who have equilibrium disorders, it is often difficult to determine the etiology of the disorders, that is, to determine whether it is dependent on a peripheral or central vestibular disorder. To attempt to guess the etiology in these cases, we devised a new method: the caloric eye-tracking pattern test. In normal subjects and in patients with peripheral disorders, as is well known, caloric nystagmus has little influence on the eye-tracking pattern. In contrast, in patients with central vestibular disorders, caloric nystagmus evoked abnormalities on the eye-tracking pattern, either superimposed or saccades, in spite of the fact that the eye-tracking pattern before the caloric stimulation is normal. These findings result from the visual suppression mechanism to the vestibular nystagmus. We can say that the visual suppression to the vestibular nystagmus is evoked more strongly bu pursuing a moving visual stimulus than by gazing at a stationary target. These results are interesting, not only form the physiological view point, but also from the clinical view point. There is a possibility of the differential diagnosis between peripheral and central vertigo.
Three cases of acute carbamazepine intoxication were evaluated neurotologically and neurologically. Findings included symptoms of equilibrium, gait and speech disorders, drowsiness, gaze nystagmus, depressed optokinetic nystagmus and disturbances of smooth pursuit eye movement. These findings, suggestive of a space-occupying lesion, disappeared after the cessation of the medication. On the basis of the clinical findings it is felt that carbamazepine affects structures within the brain stem and the cerebellum. It is well known that equilibrium disorders caused by anticonvulsant intoxication are due to cerebellar disorders, but from our present study it should be noted that they originate not only from cerebellar lesions but also from brain stem lesions.
The influence of alcohol on the oculomotor system was observed by means of the caloric eye tracking pattern (CETP) test, the visual suppression test on caloric nystagmus, and the positional nystagmus, eye tracking and gaze nystagmus tests. In Group A (nine cases whose CETP before the intake of alcohol was normal), the influence of alcohol consumption appeared regularly and consistently in the following order: abnormality of CEPT greater than or equal to positional alcohol nystagmus greater than or equal to abnormality of the eye tracking pattern greater than or equal to alcohol gaze nystagmus. On the contrary, in Group B (eight cases whose CETP before the consumption of alcohol was already abnormal), with one exception, the regularity noted in Group A was not observed. This phenomenon may be attributable to the presence of latent disorders of the oculomotor system. In both groups, the duration of the caloric nystagmus itself was slightly shortened and its amplitude somewhat suppressed after the consumption of alcohol. The results were confirmed by experiments in which the subjects kept their eyes open in darkness. On the other hand, when the eyes were kept open in light surroundings, the duration and amplitude of the caloric nystagmus were exaggerated in appearance because the mechanism of visual suppression was disturbed by alcohol.