[Circular eye tracking test (CETT)--the first report--simultaneous recording of horizontal ETT and vertical ETT, decrease of artifacts (author's transl)].
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Biomedical subjects
Publications and source records attributed to Y Umeda.
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Almost all of the conventional clinical reports on the eye-tracking test are made on the horizontal component of the smooth pursuit function of oculomotor system; few are made on the vertical component. One reason is that during the conventional vertical eye-tracking test the artifacts caused by movement of the upper eyelids often make it difficult to analyze the data. To overcome this problem the authors have developed a method to record simultaneously the horizontal and vertical components of eye movement in the eye-tracking test, and moreover, to reduce artifacts as much as possible. Our method, the circular eye-tracking test, is performed by means of an apparatus that provides a visual stimulus drawing a circle clockwise, at a rate of 120 degrees/sec, with a radius of 25.5 cm, and viewed at a distance of 70 cm.
We have identified and characterized specific binding for calcitonin gene-related peptide (CGRP) in mouse T lymphocytes. The binding of 125I-CGRP to mouse lymphocytes was reversible and the rate of dissociation of 125I-CGRP increased with the addition of the guanine triphosphate nucleotide analog, Gpp(NH)p. Saturation experiments, and Scatchard analysis indicated two classes of binding sites for CGRP; the apparent dissociation constants (KD) were 3.5 X 10(-10)M for high affinity binding sites (Bmax, 265 sites/cell) and 4.8 X 10(-8)M for low affinity binding sites (Bmax, 13,000 sites/cell). The KD value for the high affinity binding sites is roughly comparable to the IC50 and ED50 values for inhibition of T lymphocyte proliferation and increase in the cyclic AMP concentration in these cells, respectively. 125I-CGRP bound to mouse T lymphocytes was displaced by unlabeled CGRP with an IC50 value of 3.2 X 10(-10)M; salmon or human calcitonins did not inhibit the specific binding up to 1 X 10(-6)m. Our studies suggest that CGRP may be an important immunoregulatory molecule, and implicate it in the regulation of T cell function.
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In conscious rats with near-malignant phases of DOCA-salt (DS) hypertension, hemodynamics were studied with microspheres before and after administration of a vasopressin (VP) vasopressor antagonist in relation to plasma VP levels (pVP). Compared to the controls, the DS rats showed significant elevations in mean arterial pressure (MAP), total vascular resistance (TVR), and pVP, and a flow redistribution from kidney and spleen to skeletal muscles and heart, with increased vascular resistance in almost all organs. The antagonist elicited no significant systemic hemodynamic effects in DS rats as a whole; however, two subgroups, responders vs nonresponders, were identified according to the effects on MAP. In responders with a pVP of 29.2 +/- 2.7 (SE) pg/ml, the antagonist lowered MAP (-24.9 +/- 5.9 mm Hg) and TVR significantly, while in nonresponders with a pVP of 15.2 +/- 3.4 pg/ml, there were no effects. The major antagonist-induced regional responses were increased flow and decreased vascular resistance in skeletal muscles and skin in whole DS rats, and additionally in the gastrointestinal tract, portal organs, and testes in the responders. Significant correlations were observed between pVP, MAP, TVR, and depressor responses to the antagonist only when all data for DS and control rats were pooled. Thus, the systemic hemodynamic effects of VP are important only in responders with exceedingly elevated pVP. VP contributes significantly to the regional hemodynamic abnormalities in skeletal muscles and skin in whole DS rats, and also in several other organs in the responders.
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.
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Quantitative assessment of the electronystagmogram of the eye-tracking test (eye-tracking pattern) was undertaken in 20 normal subjects and 70 patients with vertigo. The abnormal recordings, contrary to the normal, showed, in varying degrees, remarkable irregularties of eye speed. These irregularties appeared in the form of spikes on the electronystagmogram at the time constant of 0.03 second. We measured the height of the spikes using 40 degrees/sec as a unit added the units of spikes appearing during a nine-second period to obtain the total index. Total indices ranged from zero (normal) to 40 + (severely abnormal), and their values showed levels of abnormality in the eye-tracking pattern more accurately than the visual analysis in current use. Standardization of the eye-tracking test, especially of the target velocity, is required for the purpose of comparing abnormalities of eye-tracking patterns recorded in different clinics. In considerations of the results of several good reports on target velocities, we have the following remarks: 1) The maximum velocity of a target which normal subjects can follow without delay of the eye movement is about 20 degrees/sec. 2) When pursuit eye movements of normal subjects are registered with the aid of an electronystagmography, the eye-tracking patterns will remain normal at target velocities of up to 45 degrees/sec. 3) In order to detect abnormalities of pursuit eye movement with the aid of an electronystagmograph, the target velocity should be as fast as possible, but not exceeding 45 degrees/sec. As an instrument for the examination of pursuit eye movements, for reasons outlined in the text, the Umeda circular eye-tracking test apparatus (amplitude 40 degrees, frequency 0.33 Hz, and target veolocity 42 degrees/sec) is ideal. The target amplitude and technical problems in making the apparatus also are discussed.