Faculty Bibliography

A stimulus consisting of 96 red LEDs mounted in the rear of a ganzfeld bowl was used to elicit focal electroretinograms (FERG) from the central 9 degrees of the retina in human subjects. The luminance of the stimulus was driven sinusoidally at frequencies from 10-60 Hz. The temporal responsiveness and response phase lags of normal subjects and patients with retinal disease were measured. Normal subjects produced maximum amplitude FERG responses to stimuli between 30-40 Hz. Patients with retinitis pigmentosa showed a low-pass pattern of amplitude loss, with an additional frequency independent loss in sensitivity in those with poorer visual acuity. Patients with macular degeneration showed general amplitude loss associated with a relative sparing of the mid-temporal frequencies. The response phase lags in both patient groups were not significantly different from the normals. These findings point to a loss in temporal responsiveness accompanied by a secondary loss of sensitivity in these heredoretinal degenerations

Temporal modulation transfer functions (MTF's) were recorded from the macula of nine normal subjects using focal electroretinography (FERG). An array of light emitting diodes (LED's) was used to experimentally manipulate stimulus temporal frequency, modulation depth, and mean luminance values. Two techniques were used to derive FERG modulation thresholds at several temporal frequencies: conventional averaging with extrapolation to a criterion amplitude, and a swept stimulus lock-in retrieval method. These two methods produced comparable results. The electrophysiologically derived MTF's were similar in shape to those obtained psychophysically. Six patients with retinal disease were also examined; all patients showed sensitivity losses which were most marked at the higher frequencies. Such losses tended to be greater in patients with poorer visual acuity

Contrast thresholds and acuity limits were measured in 4 observers with the swept visual evoked potential (VEP) technique. In this technique, grating contrast or grating spatial frequency is electronically varied while the subject's evoked response is retrieved in real time (without averaging). Contrast or spatial frequency variation make the stimulus vary in intensity; zero VEP response amplitude indicates the threshold intensity. Large shifts occur in the indicated threshold when stimulus sweep direction is reversed. Thresholds are always relatively elevated when the run begins with the strongest stimulus value. These shifts do not have a technical origin in the delay of the instrument (Nelson et al. 1984b). Here, it is shown that the shifts are due to orientation and spatial frequency selective adaptation, probably of cortical origin. Measureable adaptation is produced by momentary exposure to contrasts as low as 1.25%; nearly maximum adaptation (0.6 log units) is reached with 20% contrast. These findings support the concept of a contrast gain control mechanism in visual cortex, and pose practical problems for visual assessment with the evoked potential

We discuss the use of synchronous-demodulation (lock-in) techniques for evoked potential retrieval. Application to electronically swept visual displays is emphasized. These techniques permit a visual threshold to be specified in 20 s, but their application to visual assessment requires careful consideration of several problems, notably alleged delay in the instrumentation, specification of the baseline response level, and the nature of EEG interference. In addition, since stimulus waveform information is lost in all lock-in methods, questions concerning what activity is contributing to the measured response must be answered. A technique addressing these issues and combining phase-sensitive detection and vector computation is presented

Various noninvasive test procedures were used to evaluate retinal function in a patient who had become night blind following vincristine chemotherapy. The results obtained were strikingly similar to those reported previously in subjects with recessively inherited stationary night blindness; the dark-adaptation curve was monophasic (ie, no evidence of a scotopic branch), rhodopsin kinetics were entirely normal, and spectral threshold data revealed the presence of residual rod-mediated vision. Also like the heritable condition, the b-wave of the ERG was depressed grossly despite normal a-wave potentials. These findings, and the fact that vincristine is known to disrupt the structural integrity of neuronal microtubules, suggest that the drug-induced defect involves the process of synaptic transmission between the photoreceptors and their second-order neurons

Electrophysiologic contrast sensitivity functions (CSF) have been estimated using lock-in amplifier signal retrieval of the visually evoked response (VER). These CSFs were compared with CSFs obtained psychophysically using the same stimulus conditions. The two measures of contrast sensitivity behave similarly in response to variations of temporal and spatial frequency. The major advantage of using real-time retrieval is speed. Threshold for a single spatiotemporal condition can be estimated in as little as 20 sec, making the application of electrophysiologic contrast sensitivity testing feasible for clinical populations

Multiple sclerosis can produce highly selective losses in visual function. Psychophysical studies have demonstrated contrast sensitivity deficits for spatial frequencies or for stimulus orientations. Using real-time lock-in retrieval of the visual evoked potential, the authors measured contrast sensitivity in 15 cases with probable or definite multiple sclerosis and acuities of 20/40 or better. Sine-wave grating contrast threshold determinations for three spatial frequencies (1, 4, and 8 cycles/deg) and four orientations (0, 45, 90, and 135 deg) revealed contrast deficits in at least one spatial frequency and orientation in every case. In most cases the visual losses were spotty or multifocal, and not the same in both eyes. Some cases with highly selective patterns of orientation or spatial frequency losses were observed and are discussed in terms of involvement of cortical functional architecture in the disease