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Diabetic retinopathy has long been considered to be a retinal manifestation of systemic diabetic angiopathy. Indeed, it is therapeutically true. However, the prolongation of OP peak latency in diabetic eyes without any angiographic evidence of angiopathy leads us to presume that certain neuronal disorders occur early in diabetic eyes. Even though we cannot neglect the possibility that the prolongation of the OP peak latency may derive from undetectable retinal hypoperfusion, it is still far from conventional diabetic angiopathy. Rather, the status should be properly termed "intraretinal diabetic neuropathy" in that the neurones are the disturbed cells to cause visual dysfunction. Thereafter, the OP amplitude diminishes as retinopathy advances, probably depending on the degree of retinal circulatory disturbance. Marked diminution of the OP amplitude predicts rapid progression and poor prognosis of retinopathy. Diabetic retinal pigment epitheliopathy as manifested by one of our non-photic EOG responses is another kind of early ocular involvement of diabetes. Because its mechanisms are not yet known, so far we have not succeeded in correlating it to any kind of subjective visual index. Routine fundus inspection or fluorescent fundus angiography is incapable of detecting the compromised neural retina and/or retinal pigment epithelial integrity and thus the electrophysiology of vision has the edge in ophthalmology.

Peak latencies of pattern electroretinogram (PERG) were compared between glaucomatous eyes and non-glaucomatous eyes. Contrast threshold for motion perception (CTMP) was also measured with a new device in addition to routine static contrast sensitivity, static visual field and visual acuity. In the present recording, configurations for PERG, i.e. low reversal rate, low mean luminance and presence of background illumination, the PERG peak and trough (P1 and N2, respectively) latencies, were significantly prolonged in the glaucomatous eyes. Although both of the two PERG latencies were strongly correlated with the CTMP, only the P1 peak latency was strongly correlated with the perimetric indices. These results suggest that the P1 and N2 latencies reflect different aspects of signal processing in the retina, especially for moving targets.

The spectral sensitivity of the rapid off-response in the electroretinogram was studied in monozygotic female twins. One case was diagnosed as congenital deuteranomaly, and the other was normal. The log ratio of the sensitivity at 480 nm to the sensitivity at 620 nm (log S480/S620) was within the deutan range in the first case and within the normal range in the second. The two case were determined to be different at the retinal receptor level by study of the rapid off-response. This result of the rapid off-response was consistent with the results of the psychophysical examinations.

The scotopic threshold response (STR) is a newly investigated component of the electroretinogram. Since the STR reflects post-photoreceptoral processing in the retina at intensities near absolute threshold, the STR would be a useful index to evaluate the rod pathway in the proximal retina. A conventional ERG setup, however, involves difficulties in STR recording. Therefore we constructed a new recording system for the purpose. The characteristics of the apparatus are as follows: 1) A diffusing sphere provides full-field stimuli ranging from a very dim light near absolute threshold to a very bright light. 2) A remote-control system for changing filters is used to avoid breakdown of the dark-adapted status. 3) A software artifact rejection routine is used to exclude responses influenced by eye movements and blinks. Using the apparatus we have examined the human STR and generally confirmed the previous findings.

The effects of ceftazidime (CAZ) and flomoxef sodium (FMOX) on the in-vitro electroretinogram (ERG) of albino rabbits were studied. The a-wave, the b-wave and the oscillatory potential (OP) were unchanged by 0.3mM (0.19mg/ml) CAZ-containing solution. The OP was suppressed by 0.5mM (0.32mg/ml) CAZ. The a-wave, the b-wave and the OP were unchanged by 0.5mM (0.26mg/ml) FMOX. The OP was suppressed and its peak latency was delayed by 2mM (0.52mg/ml) FMOX. The concentration of 0.3mM (0.19mg/ml) CAZ was higher than its minimum inhibitory concentration (MIC) against Staphylococcus aureus, Staphylococcus epidermidis, Pseudomonas aeruginosa, Serratia marcescens and Propionibacterium acnes. The concentration of 0.5mM (0.26mg/ml) FMOX was higher than its MIC against Staphylococcus aureus, Staphylococcus epidermidis, Serratia marcescens and Propionibacterium acnes.

We evaluated the retinal toxicity of antimicrobials (sulbenicillin, cefazolin, flomoxef, gentamicin, sisomicin, netilmicin, tobramycin, amikacin, vancomycin, ofloxacin, lomefloxacin, and miconazole) by the electroretinogram, before and after a single-shot intravitreal injection in rabbits. The clinical dosage for single-shot intravitreal injections which we recommend are 2 mg for sulbenicillin, 0.25 mg for cefazolin, 0.2 to 0.4 mg for flomoxef, 0.1 mg for gentamicin, 0.1 to 0.2 mg for netilmicin, 0.2 to 0.4 mg for amikacin, 0.2 mg for tobramycin, 1 mg for vancomycin, 0.2 mg for ofloxacin, 0.2 mg for lomefloxacin, and 0.05 mg for miconazole.

The depth profiles of the b- and d-waves of the electroretinogram were studied in the isolated frog retina placed with its receptor side up. The electrode was introduced into the retina from the receptor side and the reference electrode was placed on the vitreal side. The b-wave was maximum in amplitude in the receptor layer, and decreased as the electrode was advanced proximally from the outer plexiform layer until it disappeared at the inner limiting membrane. The b-wave in the inner plexiform layer was different from that in the distal portion of the inner nuclear layer in form and peak latency. The results suggested that the b-wave is generated in the layers between the inner limiting membrane and the outer plexiform layer, and that at least two processes are involved in the generation of the b-wave. The depth profile of the d-wave resembled that of the b-wave except in the receptor layer; it was recorded in the whole retinal layers as was the b-wave, and decreased as the electrode was advanced proximally until it disappeared at the inner limiting membrane. The peak latency of the d-wave was longer in the inner plexiform layer than in the distal portion of the inner nuclear layer. The results indicated that the d-wave consists of the off-response of the late receptor potential and the postsynaptic components, the latter being generated by a similar mechanism as the b-wave.

The electroretinographic rapid off-response, composed mainly of the late receptor potential of cones, is found to be abnormal in all protans and deutans so far tested. The rapid off-response can thus be used as an objective measure in the diagnosis of congenital red-green colour defect.

Correlation between the electroretinographic oscillatory potential and psychophysical contrast sensitivity function was examined in patients with different stages of diabetic retinopathy. Contrast sensitivity function was evaluated by Arden's grating test. The amplitude of the oscillatory potential was significantly reduced in cases with low contrast sensitivity (P less than 0.01).

The effects of penicillin G (PC-G) sodium, procaine PC-G, cloxacillin sodium (MCIPC), disodium sulbenicillin (SBPC), cefazolin sodium (CEZ), gentamicin sulfate (GM) and fosfomycin sodium (FOM) on the electroretinogram (ERG) of the human in-vitro eye-cup were studied. The oscillatory potentials (OPs) were selectively and greatly suppressed by 1.0 mM PC-G sodium. The OPs and c-wave were suppressed by 0.85 mM procaine PC-G. The b-wave and OPs were slightly suppressed by 1.0 mM MCIPC. The a-wave, b-wave, OPs and c-wave were not deteriorated by 1.0 mM SBPC. The OPs appeared to be selectively suppressed by 1.0 mM CEZ. The b-wave was suppressed and the peak latencies of the OPs were delayed by 184 micrograms/ml (approximately 0.4 mM) GM. The amplitudes of the a-wave and c-wave were slightly enhanced and their peak latencies were slightly delayed by 184 micrograms/ml GM. The a-wave, b-wave, OPs and c-wave were not deteriorated by 1.0 mM FOM. The results of the present study on the human retina were comparable to those on the albino rabbit retina in our previous studies.

Toxicity of an intravitreal injection of gentamicin sulfate, disodium sulbenicillin and cefazolin sodium on the retina was investigated by electroretinogram in albino and pigmented rabbits. Recordings were made before injection and 2 hours and 3, 7, 14, and 21 days after injection. Significant differences were found in the susceptibility of the electroretinogram components to various antibiotics as follows. Gentamicin 0.24 mg/0.1 ml irreversibly abolished all the components examined. Sulbenicillin 4.0, 8.0, or 12 mg/0.1 ml transiently suppressed the b-wave and the oscillatory potentials incrementally with increasing dose. Cefazolin 0.5, 2.0, or 5.0 mg/0.1 ml selectively reduced the oscillatory potentials, leaving the a- and b-waves almost unattenuated. The cefazolin-suppressed oscillatory potentials recovered within 14 days after injection. Judging from the most susceptible electroretinogram components to each antibiotic, we recommend intravitreal doses of these antibiotics for clinical use as follows: gentamicin 0.1 mg/0.1 ml, sulbenicillin 2 mg/0.1 ml, and cefazolin 0.25 mg/0.1 ml.

Stargardt's disease-fundus flavimaculatus has four general distribution patterns in fundus appearance: (1) macular degeneration without flecks; (2) macular degeneration with perifoveal flecks; (3) macular degeneration with diffuse flecks; and (4) diffuse flecks without macular degeneration (Noble and Carr, 1979). Four cases corresponding each to the four subgroups were studied electrophysiologically by our new tests for the cone receptor cell (rapid off-response in the ERG) and for the retinal pigment epithelium (the hyperosmolarity response and the Diamox response). The results of our electrophysiological tests appear consistent with the histological findings by Klien and Krill (1967) and by Eagle et al. (1980), showing that the primary defect of fundus flavimaculatus is in the retinal pigment epithelium. Electrophysiologically, the severity of the disease correlated well with each fundus pattern.

The depth profile of the electroretinographic oscillatory potentials was studied in the isolated frog retina. The intraretinal electrode was introduced from the receptor side, and the reference electrode was placed on the vitreal side. The electroretinogram, recorded either transretinally or with the electrode tip in the receptor layer, showed 4 to 10 oscillatory potential wavelets. As the electrode was advanced proximally, the wavelets disappeared as a function of retinal depth. The wavelets with longer peak latencies disappeared earlier, and only the first one or two wavelets could be identified when the electrode was in the inner plexiform layer. These findings indicate that the oscillatory potentials are generated between the inner and outer plexiform layers and that the earlier wavelets originate in the more proximal retina. The results are consistent with the notion that the oscillatory potentials are generated by synaptic feedback circuits.

New clinical methods are proposed to assess (1) neuronal activities of the retinal inner layers including amacrine cells by means of the oscillatory potential, (2) photopic function through the rapid decay in the off-response and (3) activities of the retinal pigment epithelium through susceptibility of the standing potential of the eye to osmotic stress and to Diamox. These new methods are able to reveal otherwise undetectable retinal disorders.