Scoptopic visibiity curve in man obtained by the visual evoked response.
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Biomedical subjects
Publications and source records attributed to E Adachi-Usami.
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We examined temporal frequency curves by pattern visual evoked potential in 28 eyes suffering from retinitis pigmentosa (RP). The peak latency of the P100 component was 110.3 +/- 3.0 msec (S.E.), which was not significantly different from the 110.2 +/- 0.8 msec (S.E.) obtained from 60 normal controls. The P100 amplitudes of whole reversal frequencies, however, were decreased in patients with RP (p less than 0.05), especially at lower frequencies. We thought this phenomenon was useful for determining central visual function in patients with RP.
We developed a new visual stimulating system for recording visual evoked cortical potentials and electroretinograms. The stimulus was a color checkerboard, in which each check kept its chromaticity but changed its luminance with its corresponding check. Color-coded pattern stimuli using red and green checks did not produce visual evoked cortical potentials, while yellow checks produced clear responses in a normal subject. Moreover, five color stairs from red and green to yellow showed only that the more colors are different, the smaller the visual evoked cortical potentials become. In addition electroretinogram recordings indicated that color-coded patterns behave in the same way as in visual evoked cortical potentials. The mechanism that causes the small color visual evoked cortical potentials may already be present in the retina. Color perception may be able to induce a suppression of responses for luminance contrast that appears to be formed already in the retina. Retinal responses were affected whether the stimulus field was color coded or not. Pattern electroretinograms appear to be more than the sum of local on and off responses.
To evaluate the retinal toxicity of mitomycin C injection in the rat eye, we conducted an electroretinographic study and a histopathologic study. Three different concentrations of mitomycin C (0.2, 0.3 and 0.4 mg/ml) were injected into either the vitreous cavity or the anterior chamber of the experimental eyes. A full-field electroretinogram was recorded before injection and 2, 4 and 7 days after injection. The retinas of all eyes were examined by light and electron microscopy. We found no evidence of electroretinographic and histologic changes 2 and 7 days after injection of 0.4 mg/ml of mitomycin C into the anterior chamber. However, profound electroretinographic changes did follow injection of the drug into the vitreous. These were absent with the 0.2-mg/ml solution at 7 days, mild with the 0.3-mg/ml solution at 7 days and profound with the 0.4-mg/ml solution as early as 2 days. Intravitreal injection of 0.4 mg/ml, however, showed selective degeneration of Müller cell process at day 2, retinal pigment epithelium changes at day 4 and irregular arrangement of the outer nuclear layer and photoreceptors at day 7. Intravitreal injection of mitomycin C in a concentration comparable to the one used clinically could cause retinal disorders, both functionally and histologically.
Electrophysiologic findings including multifocal electroretinogram and visual evoked cortical potentials were studied in a patient with multiple evanescent white dot syndrome. A 19-year-old woman was diagnosed as having multiple evanescent white dot syndrome because of decreased visual acuity, white dots on fundus examination and hyperfluorescence of the white dots in the right eye. The amplitude of the flicker electroretinogram was reduced, but the single-flash electroretinogram was within the normal range. The P100 latency of the pattern visual evoked cortical potentials was slightly prolonged. The amplitudes of multifocal electroretinogram were markedly reduced in the area corresponding to the scotoma and moderately reduced in other regions of the central field in the affected eye. The results suggest that the retinal dysfunction area is wider than that detected by subjective methods or conventional electrophysiological examinations. The delayed recovery of the visual evoked cortical potential latency suggests the involvement of the optic nerve in multiple evanescent white dot syndrome.
PURPOSE: Electrophysiological evaluation of the visual function of patients with toxic neuropathy caused by toluene abuse. METHODS: Fifteen patients (mean age 25.6 years, eight men and seven women) were diagnosed with bilateral optic neuropathy. Pattern visual evoked cortical potentials (PVECPs) and clinical symptoms were investigated. RESULTS: Visual acuities at the initial visit were less than 0.1 in 5 cases and 0.1-1.0 in 10 cases. PVECPs were followed up in the 15 cases. At the first recording, PVECPs were nonrecordable in both eyes of 11 cases, the P100 peak latency was prolonged in both eyes of 3 cases, and only 1 case showed a normal P100 peak latency. After treatment, visual acuities improved more than 2 lines in 6 cases, 3 of whom showed normal P100 peak latency in the PVECPs. Visual prognosis and PVECP changes were identical in both eyes of all patients. CONCLUSIONS: In patients with toluene optic neuropathy, the P100 peak latency of PVECP shortened as visual acuity improved. The VECP abnormalities in these patients suggest that there is a severe effect on the optic nerve after prolonged exposure to toluene.
PURPOSE: To relate the electrophysiological changes in the retina induced by the excitatory neurotoxin, kainic acid (KA), to its receptor sites in the rat. METHODS: Fifty-five Wistar rats were injected intravitreally with 100, 50, 25, 12.5, 6.25, 3.12, or 1.56 nmol of KA. The electroretinograms (ERGs) including oscillatory potentials (OPs) elicited by a series of increasing intensities were recorded before, and 6 hours, 1 day, 1 week, and 1 month after the injection of KA. RESULTS: After KA injection, the a-waves showed no significant change at all intensity levels (P > .05), but the amplitudes and implicit times of the b-wave were significantly altered. The abolition of the b-wave by KA resulted in a negative response, which decreased progressively with time. The implicit times of the b-wave showed a marked prolongation after injection of 100 nmol of KA (P < .01). The OPs disappeared at the KA dose of 6.25 nmol and higher; doses of 1.56 to 3.12 nmol of KA depressed the Ops. CONCLUSIONS: We conclude that KA altered the above-mentioned ERG components in a dose-dependent manner. These alterations of the ERG can be explained by alterations of neurons in the inner retinal layers.
The effect of an intravitreal injection of ornithine on the retina of rats was studied electroretinographically. Rats were injected intravitreally with 5 microl of 0.02, 0.25 and 0.5 M ornithine. Electroretinograms (ERGs) were recorded before, and 1, 3 and 9 days after the injection. High doses of ornithine (0.5 M) reduced while low doses (0.02 M) enhanced the ERG amplitudes. The implicit time of the a-wave was delayed at all concentrations after ornithine injection, which suggests that implicit times may be a more sensitive parameter of the ornithine effect. There were significant changes in the stimulus intensity necessary to obtain the one half of the maximum amplitude of the b-wave that may have been caused by damage of the photoreceptors and retinal pigment epithelium cells by ornithine. We conclude that the effect of ornithine on retinal function is dose dependent and can either enhance or depress the ERG amplitudes.
PURPOSE: To determine whether docosahexaenoic acid (DHA) can reduce the retinal damage induced by transient retinal ischemia. METHODS: Retinal ischemia was induced by increasing intraocular pressure (IOP). Retinal circulation was restored by lowering IOP. An intraperitoneal injection of 1,000 mg/kg of DHA-ester (DHA-E) was given 5 h before the ischemia. Electroretinograms were recorded just before the ischemia and at 60-min intervals up to 4 h after circulation was restored. RESULTS: The ratio of the amplitudes after the ischemia to that just before ischemia was significantly higher in eyes administered DHA-E than in controls at each time point (p < 0.01). CONCLUSION: DHA-E is effective in protecting the retina against transient retinal ischemia.
PURPOSE: To verify the efficiency and objectivity of the pattern visual evoked potential (VEP) for organic disorders of the cortical visual system. METHODS: This retrospective study evaluated VEP in 19 patients diagnosed with psychogenic visual disturbance, 7 patients with malingering, and 37 age-matched normal volunteers. Transient (3 reversals per second) and steady-state (12 reversals per second) pattern VEPs for check sizes 15' and 30', with a contrast of 80%, were recorded. RESULTS: The amplitudes of both transient and steady-state pattern VEPs were significantly increased in patients with psychogenic visual disturbance, while patients with malingering had significantly lower amplitudes. P100 peak latency was prolonged in both groups of patients. CONCLUSION: Monitoring of patients' fixation on the stimulus showed those with psychogenic visual disturbance fixated well on the stimulus, while those with malingering did not. This finding produced a VEP amplitude reduction in patients with malingering. The reason for the VEP amplitude in patients with psychogenic visual disturbance is unclear.