Luminance Flicker Research Articles

Attention-capturing properties of high frequency luminance flicker: Implications for brake light conspicuity

Abstract In two experiments, the authors studied the effect of high frequency luminance flicker on reaction time in a simulated driving task. In Experiment 1, 24 research participants performing a primary simulated driving task were required to apply the brake pedal as quickly as possible following the activation of a red light somewhere in their field of vision. The red lights were displayed in one of two ways, (a) with 20 Hz luminance flicker and (b) continuous (no flicker), and presented at three eccentricities, 10°, 45° and 80°. Results showed that the light with 20 Hz flicker was more attention-capturing than the continuous light, but that the effect of 20 Hz flicker on reaction time was not influenced by eccentricity of presentation. The second experiment was identical to the first except that the primary simulated driving task was considerably more attention demanding. Under this higher workload, the light with 20 Hz flicker again proved to be more attention-capturing than the continuous light, and to a greater extent than in Experiment 1. In Experiment 2, there also appeared to be tendency for the light with 20 Hz flicker to be more effective at greater eccentricities. Implications for brake light conspicuity and rear-end collision avoidance are discussed.

Color vision deficiency in retinitis pigmentosa

PurposeThis study examined which color vision test was superior in the detection of acquired color vision deficiencies and the relative magnitudes of red–green (RG) and blue–yellow (BY) discrimination losses in retinitis pigmentosa (RP). MethodsColor vision examinations were conducted using Standard Pseudoisochromatic Plates Part 2 (SPP Part 2) and a flicker threshold test (TMT) in 21 RP and 21 age- and sex-matched normals. The TMT test consists of luminance, BY and RG flicker tests. Relative Operating Characteristic analysis (ROC) was used to determine the effectiveness of each test. Bigger ROC area gain and high performance (%) indicate a better test. Regression and correlation analyses were used to determine the relative magnitudes of RG and BY discrimination losses for the SPP Part 2. For TMT the findings were represented graphically where the mean log sensitivity was plotted against the frequency of mean luminance; RG and BY flicker individually and the range was plotted with the 5th and 95th percentile. ResultsBoth tests were able to determine BY and RG acquired color vision deficiencies in RP patients. SPP Part 2 showed the highest area gain (0.39) and performance (78%). The TMT generally showed less area gain and performance compared to SPP Part 2. Pearson's correlation coefficient analysis on the RG and BY SPP Part 2 test plates showed a strong relationship (r=0.96, p<0.0001) between RG and BY discrimination losses suggesting that RP patients suffer roughly equal losses in RG and BY discrimination. Analysis of the TMT also showed an equal loss of sensitivity across all the frequencies in all three tests suggesting an overall reduction of sensitivity confirming the non-specific frequency and non-color specific loss. ConclusionsThe SPP Part 2 appears to be a superior test compared to TMT in detecting acquired color vision deficiencies in RP patients. RP subjects also suffer both RG and BY acquired color vision deficiencies.

Spectrally opponent inputs to the human luminance pathway: slow +M and −L cone inputs revealed by intense long‐wavelength adaptation

The nature of the inputs to achromatic luminance flicker perception was explored psychophysically by measuring middle- (M-) and long-wavelength-sensitive (L-) cone modulation sensitivities, M- and L-cone phase delays, and spectral sensitivities as a function of temporal frequency. Under intense long-wavelength adaptation, the existence of multiple luminance inputs was revealed by substantial frequency-dependent changes in all three types of measure. Fast (f) and slow (s) M-cone input signals of the same polarity (+sM and +fM) sum at low frequencies, but then destructively interfere near 16 Hz because of the delay between them. In contrast, fast and slow L-cone input signals of opposite polarity (-sL and +fL) cancel at low frequencies, but then constructively interfere near 16 Hz. Although these slow, spectrally opponent luminance inputs (+sM and -sL) would usually be characterized as chromatic, and the fast, non-opponent inputs (+fM and +fL) as achromatic, both contribute to flicker photometric nulls without producing visible colour variation. Although its output produces an achromatic percept, the luminance channel has slow, spectrally opponent inputs in addition to the expected non-opponent ones. Consequently, it is not possible in general to silence this channel with pairs of 'equiluminant' alternating stimuli, since stimuli equated for the non-opponent luminance mechanism (+fM and +fL) may still generate spectrally opponent signals (+sM and +sL).

Short-Term Increase of Intraocular Pressure Does Not Alter the Response of Retinal and Optic Nerve Head Blood Flow to Flicker Stimulation

It has been shown that stimulation with diffuse luminance flicker induces vasodilatation in the human retina and increases optic nerve head (ONH) blood flow. The present study was designed to investigate the influence of a short-term increase in intraocular pressure on flicker-induced changes in ONH blood flow and retinal vessel diameters. In a group of 15 healthy volunteers, IOP was increased by the episcleral suction cup technique. ONH blood flow was assessed with a laser Doppler flowmeter, and retinal vessel diameters were measured with the retinal vessel analyzer. Flicker responses of retinal vessel diameters and ONH blood flow were determined at baseline conditions and during suction of 70 and 140 mm Hg. Flicker light consisted of 8-Hz square-wave flashes at a wavelength below 550 nm and produced a retinal irradiance of 140 muW/cm(2). Suction increased IOP from 12 +/- 2 to 27 +/- 4 mm Hg and 43 +/- 4 mm Hg. Stimulation with diffuse luminance flicker induced an increase in ONH blood flow of +24.0% +/- 20.7%. Increased IOP did not significantly change the flicker response in the ONH (+19.3% +/- 26.6% and +22.1% +/- 25.1%). In retinal veins, flicker induced an increase in vessel diameter of +3.0% +/- 2.0%. Flicker responses in retinal veins were not significantly altered after the IOP was increased, compared with those recorded at baseline IOP (+2.8% +/- 2.5% and +3.2% +/- 2.2%). The flicker response in retinal arteries at baseline IOP was +3.5% +/- 2.0%. Again, the increase in IOP did not significantly alter this flicker response (+2.8% +/- 1.6% and +3.1% +/- 2.4%). A short-term increase in IOP does not alter the response of retinal vessel diameters and ONH blood flow to diffuse luminance flicker, which indicates that increased IOP does not alter retinal or ONH regulation during neuronal stimulation.

Flicker-evoked response measured at the optic disc rim is reduced in ocular hypertension and early glaucoma.

To determine in patients with ocular hypertension (OHT) or early glaucoma (EOAG) the change in blood flow measured at the neuroretinal rim of the optic disc in response to a 15-Hz diffuse green luminance flicker, a stimulus that activates predominantly the ganglion cell magnocellular pathway. Thirteen patients with EOAG, 29 with OHT, and 16 age-matched control subjects, all with excellent fixation, were examined. Blood flow (F(onh)) at the neuroretinal rim of the optic disc was continuously monitored by laser Doppler flowmetry before and during exposure to a 15-Hz, 30 degrees field green luminance flicker. The response of F(onh) to this stimulus (RF(onh)) was expressed as percentage change in F(onh) between baseline and the last 20 seconds of flicker. Two to three temporal sites of the disc were tested, and the highest RF(onh) was considered for further analysis. RF(onh) results in patients were correlated with morphologic (cup-to-disc area ratio, cup shape neuroretinal rim area) and functional (perimetric mean deviation and pattern electroretinogram amplitude) clinical parameters. In the patients with OHT or EOAG, F(onh) and RF(onh) were both reduced compared with their respective values in the control group. Both quantities decreased significantly with neuroretinal rim area when the patients' data were pooled. No significant correlation was found between F(onh) or RF(onh) and the other morphometric and functional parameters. The group-averaged time course of RF(onh) was not significantly different from that in the normal subjects. Luminance flicker-evoked RF(onh) is abnormally reduced in patients with OHT or EOAG, indicating an impairment of neurally mediated vasoactivity. The data suggest that PERG-derived neural activity and flicker-evoked RF(onh) can be independently altered early in the disease process.

Response of retinal vessel diameters to flicker stimulation in patients with early open angle glaucoma.

Diffuse luminance flicker increases retinal vessel diameters in animals and humans, indicating the ability of the retina to adapt to different metabolic demands. The current study seeks to clarify whether flicker-induced vasodilatation of retinal vessels is diminished in glaucoma patients. Thirty-one patients with early stage glaucoma (washout for antiglaucoma medication) and 31 age- and sex- matched healthy volunteers were included in the study. Retinal vessel diameters were measured continuously with a Retinal Vessel Analyzer. During these measurements three episodes of square wave flicker stimulation periods (16, 32, and 64 secs; 8 Hz) were applied through the illumination pathway of the retinal vessel analyser. Flicker-induced vasodilatation in retinal veins was significantly diminished in glaucoma patients as compared with healthy volunteers (ANOVA, P < 0.01). In healthy volunteers, retinal venous vessel diameters increased by 1.1 +/- 1.8% (16 seconds, P < 0.001), 2.0 +/- 2.6 (32 seconds, P < 0.001), and 2.1 +/- 2.1% (64 seconds, P < 0.001) during flicker stimulation. In glaucoma patients, venous vessel diameters increased by 0.2 +/- 1.7% (16 seconds, P < 0.6), 1.1 +/- 2.1% (32 seconds, P < 0.01), and 0.8 +/- 2.5 (64 seconds, P < 0.09). In retinal arteries, no significant difference in flicker response was noticed between the two groups (ANOVA, P < 0.6). In healthy controls, flicker stimulation increased retinal arterial vessel diameters by 1.0 +/- 2.4% (P < 0.03), 1.6 +/-3.2% (P < 0.004) and 2.4 +/- 2.6% (P < 0.001) during 16, 32, and 64 seconds of flicker, respectively. In glaucoma patients, flickering light changed arterial vessel diameters by 0.3 +/-2.6% (16 seconds, P = 0.4), 1.3 +/-3.1% (32 seconds, P = 0.03), and 1.8 +/- 3.8% (64 seconds, P = 0.005). Flicker-induced vasodilatation of retinal veins is significantly diminished in patients with glaucoma compared with healthy volunteers. This indicates that regulation of retinal vascular tone is impaired in patients with early glaucoma, independently of antiglaucoma medication.

Laser Doppler instrument to investigate retinal neural activity-induced changes in optic nerve head blood flow

A fundus camera-based instrument to investigate increased retinal neuronal activity effect on optic nerve blood flow is described. It incorporates (a) near infrared fundus illumination and observation, (b) near infrared laser Doppler flowmeter (LDF), (c) pupil position monitoring and (d) delivery of visual stimuli. Two types of stimulation are currently used: diffuse heterochromatic and chromatic luminance flicker generated by light emitting diodes, and contrast reversal pattern displayed on a video monitor. Recordings of the changes in the LDF parameters (blood velocity, volume and flow) from the optic nerve in response to these stimuli illustrate the potential of the technique.

Age, blood pressure, and vessel diameter as factors influencing the arterial retinal flicker response.

The present study investigated whether age, blood pressure (BP), and baseline vessel diameter influence the retinal arterial response to flicker light. Thirty healthy subjects (mean age, 46.3; range, 22-73 years) and 15 patients with untreated essential arterial hypertension (mean, 50.9; range, 26-69 years) were examined. The diameter of the retinal arterioles was measured by a Retinal Vessel Analyzer (RVA; Imedos, Weimar, Germany). Each examination consisted of a 100-second baseline measurement and five 20-second periods of flicker stimulation, followed by an 80-second observation period. The five stimulation periods were then averaged. The rectangular luminance flicker operated at 12.5 Hz at a wavelength of 530 to 600 nm. The baseline-corrected flicker response (bFR) was defined as the difference between the peak dilatation and subsequent constriction after flicker stimulation minus the fluctuation of the baseline. The BP was measured at 1-minute intervals during the examination. In 26 subjects with normal BP, flicker light induced a bFR of +6.4% +/- 2.7%. The bFR decreased nonsignificantly in healthy subjects with increasing age (y = 8.48-0.048x; r = 0.26). The baseline diameter did not influence the amplitude of the flicker response over a range of 70 to 140 measuring units. The hypertensive patients reacted with a bFR of +2.2% +/- 2.5% (P < 0.001). Four hitherto healthy subjects with elevated BP during the examination were excluded from analysis. A significant correlation of age and bFR was not found in the small sample examined. Untreated arterial hypertension appeared to be associated with a reduced flicker response. The value of such functional vessel properties in the screening of vasosclerosis and in diagnostics in arterial hypertension should be examined in further studies.

Functional imaging of the human papilla and peripapillary region based on flicker-induced reflectance changes

A non-invasive functional imaging technique of the nervous tissue of the human eye fundus based on two wavelength light reflectance changes (Δ R %) is presented. The effect of 30° diffuse luminance flicker field made of two spectral components (569 and 600 nm) on Δ R was studied in six normal volunteers. Group averaged Δ R was significant and similar in all quadrants of the optic disc at 569 nm with a mean equal to −10.7% for the tissue of the optic disc and −3.6% for the peripapillary regions. At 600 nm, the Δ R were also significant but smaller, i.e. −3.5% for the disc tissue and −1.7% for the peripapillary region. The changes at 569 and 600 nm represent most probably blood volume changes. The 600 nm reflectance did not show evident features suggesting the presence of flicker-induced oxygenation changes.

Diffuse luminance flicker increases blood flow in major retinal arteries and veins

It has been shown that diffuse luminance flicker increases optic nerve head blood flow. The current study has been performed to quantify changes in retinal blood flow during flicker stimulation. In a group of 11 healthy volunteers, red blood cell velocity and retinal vessel diameters were assessed with bi-directional laser Doppler velocimetry and the Zeiss retinal vessel analyzer before, during and after stimulation with diffuse luminance flicker. Retinal blood flow was calculated for each condition. Flicker stimulation increased retinal blood flow by +59 ± 20% ( p<0.01) in arteries and by +53 ± 25% ( p<0.01) in retinal veins. These results demonstrate that diffuse luminance flicker increases retinal blood flow in the human retina.

Temporal dynamics and magnitude of the blood flow response at the optic disk in normal subjects during functional retinal flicker-stimulation

Near-infrared laser Doppler flowmetry was applied in 15 normal volunteers to record the time course and magnitude of changes in the velocity (Vel), volume (Vol) and flow ( F) of blood and tissue reflectance ( R) at the optic disk in response to 40 and 50 s of increased retinal neural activity. This activity was evoked by diffuse luminance flicker of the retinal posterior pole. After 20 s of flicker, the group averages of Vel, Vol, and F were significantly higher than at baseline (pre-flicker) by 12, 24 and 38%. Time constants of the increases in Vel, Vol, and F were 3.4, 12.7 and 9.1 s, respectively. The group average change in R of 1% was not significant. However, in one subject, 15 recordings from the same site of the optic disk showed a significant increase in R of 8%, with a time course similar to that of Vol. Our findings show that, in the human optic nerve, a white matter tissue, the temporal dynamics and magnitude of the response of blood flow to an increase in retinal neural activity are similar to those reported for brain gray matter. Furthermore, although the R-response could be due, in part, to changes in blood volume, other factors, such as activity-evoked tissue scattering changes, may also affect this response.

Flicker light-induced vasodilatation in the human retina: effect of lactate and changes in mean arterial pressure.

Diffuse luminance flicker light increases retinal and optic nerve head blood flow in animals and humans, but the exact mechanisms that mediate increased flow have yet to be identified. In the current study, the effect of increased plasma lactate levels on flicker-induced vasodilatation in the retina was investigated in three independent studies in healthy humans. In the first study, plasma lactate concentrations were increased by bicycle exercise in 12 volunteers, and the change in retinal vessel diameter to 8-Hz square-wave flicker stimulation was measured with the Zeiss Retinal Vessel Analyzer (Carl Zeiss Meditec, Oberkochen, Germany). In a different study, sodium lactate was administered intravenously, and flicker responses were measured in 12 subjects. As a control experiment accounting for pressure increases induced by exercise, the effect of elevated ocular perfusion pressure on the flicker response was investigated during tyramine infusion (n = 12). The increase in plasma lactate concentration during intravenous infusion from 1.3 +/- 0.4 to 6.3 mmol/L and during dynamic exercise from 1.2 +/- 0.3 to 9.4 mmol/L decreased flicker responses in retinal arteries from 5.3% +/- 0.9% to 1.7% +/- 0.6% (P < 0.001) and from 3.6% +/- 0.6% to 2.0% +/- 0.8% (P = 0.03), respectively. In contrast, an increase of mean blood pressure from 81 +/- 3 to 92 +/- 3 mm Hg after tyramine infusion had no significant effect on flicker-induced vasodilatation in retinal arteries and veins. The signaling between neuronal activity and flow response in the human retina is sensitive to changes in blood lactate levels, whereas changes in systemic blood pressure have no major effect. Whether an increased cytosolic redox impairment contributes to flicker-induced vasodilatation has yet to be clarified.

Characterization of the human visual V6 complex by functional magnetic resonance imaging.

Magnetoencephalography of a visual area along the human parieto-occipital sulcus suggested that this region represents the human homologue of the monkey visual area V6 complex (visual area V6/visuomotor area V6A) involved in the integration of visual and somatomotor information. We used functional magnetic resonance imaging at 2.0 T and 2 x 2 x 3 mm3 resolution (16 sections) to characterize visual areas along the parieto-occipital sulcus in five healthy human subjects. Paradigms comprised a full-field checkerboard stimulation, a full-field luminance flicker as well as a foveal and peripheral luminance flicker using both a direct and differential design for comparing functional states. Along the parieto-occipital sulcus, and in contrast to primary visual areas, luminance stimulation evoked much larger activation volumes than checkerboard stimulation. Moreover, based on anatomic landmarks, luminance stimulation identified two functionally distinct regions of parieto-occipital sulcus activations: an inferior part (supposedly visual area V6) and a superior portion (supposedly visuomotor area V6A). With these assignments, foveal vs. peripheral luminance stimulation revealed a weaker foveal overrepresentation in visual area V6/visuomotor area V6A than in early visual areas, and only a mild tendency for a retinotopic organization in visual area V6. Further analyses of the functional coding of the human visual area V6 complex require functional magnetic resonance imaging at even higher spatial resolution.

Adaptation from invisible luminance and chromatic flicker

Adaptation from invisible luminance and chromatic flicker

Flickering light increases retinal blood flow.

To examine the retinal blood flow in normal eyes before and during retinal stimulation by flickering light. A prospective cross-sectional study. PARTICIPANTS AND TESTING: Twenty-seven eyes of 27 normal subjects with a mean age +/- SD of 38 +/- 15 years (study I) and 21 eyes of 21 normal subjects with a mean age +/- SD of 46 +/- 17 years (study II) were examined with respect to capillary retinal blood flow and central retinal artery and central retinal vein blood flow velocities during flickering light stimulation. A luminance flicker light with a frequency of 8 Hz increased the neuronal activity of retinal ganglion cells. In study I, the retinal capillary blood flow was measured before and during flickering by scanning laser Doppler flowmetry (670 nm, Heidelberg Retina Flowmeter). In study II, the blood flow velocities in the central retinal artery and central retinal vein were examined by pulsed Doppler sonography. Change in blood flow velocities in the central retinal artery and vein and in retinal capillary blood flow after full-field flicker stimulation. In study I, measurements of blood flow during retinal flicker stimulation showed a significant increase in the mean value of blood flow +/- SD from 317 +/- 72 arbitrary units to 416 +/- 103 arbitrary units. The change was on average 46 +/- 19%. In study II, the systolic and end-diastolic blood flow velocities in the central retinal artery increased significantly (P < 0.0001): systolic, 9 cm/s to 15 cm/s (+62%); end-diastolic, 2.7 cm/s to 5.3 cm/s (+96%). In the central retinal vein, the systolic and end-diastolic blood flow velocities increased significantly (P < 0.0001): systolic, 4.3 cm/s to 6.7 cm/s (+56%); end-diastolic, 1.8 cm/s to 3.6 cm/s (+100%). The authors found no significant change in blood pressure and heartbeat frequency. Visual stimulation of the retina by flickering light strongly increased the juxtapapillary retinal capillary blood flow and central retinal artery blood flow velocity in normal eyes.

Influence of diffuse luminance flicker on choroidal and optic nerve head blood flow

Purpose. In the retina there is general agreement that blood flow adapts in response to different conditions of light and darkness including diffuse luminance flicker. By contrast, regulation of choroidal blood flow in response to different light conditions is still a matter of controversy. Thus, we investigated the effect of diffuse luminance flicker on choroidal and optic nerve head blood flow. Methods. In a group of 14 healthy volunteers, choroidal blood flow and ocular fundus pulsation amplitude were assessed with laser Doppler flowmetry and laser interferometry, respectively. Measurements were done before, during and after stimulation with diffuse luminance flicker. Furthermore, the response of optic nerve head blood flow (ONHBF) to flicker stimulation was measured. Flicker stimuli were generated by a Grass® PS2 photostimulator, stimulating at a frequency of 8 Hz. Flicker light consisted of light flashes at a wavelength below 550nm and produced a retinal irradiance of 140 µW/cm 2. Blood pressure and pulse rate were measured non-invasively. Paired t-test was used for statistical analysis. Results. ONHBF increased immediately after onset of flicker stimulation. The maximum increase in ONHBF was 30% ± 10% (mean ± SEM, p < 0.008). Both choroidal perfusion parameters were only slightly increased during flicker stimulation, by 2 ± 2% (laser Doppler flowmetry, p < 0.5) and by 4 ± 1% (laser interferometry, p < 0.12). After the end of stimulation all values returned to baseline levels. Conclusion. Our study clearly demonstrates that diffuse luminance flicker increases optic nerve head blood flow. In contrast, increased neural activity in the retina has no effect on choroidal blood flow. Thus, choroidal blood flow appears to be largely independent of alterations in retinal metabolism.

Processing of second-order motion stimuli in primate middle temporal area and medial superior temporal area.

Two rhesus monkeys were subjects in a direction-discrimination task involving moving stimuli defined by either first- or second-order motion. Two different second-order motion stimuli were used: drift-balanced motion consisting of a rectangular field of stationary dots and theta motion consisting of the same rectangular field with dots moving in the direction opposite to that of the object. The two types of stimuli involved different segmentation cues between the moving object and the background: temporal structure of the luminance (flicker) in the case of drift-balanced motion and opposed motion in the case of the theta-motion stimulus. Our monkeys were able to correctly report the direction of each stimulus. Single-unit recordings from the middle temporal (MT) and medial superior temporal (MST) areas revealed that 16 out of 38 neurons (41%) from area MT and 34 out of 68 neurons (50%) from area MST responded in a directionally selective manner to the drift-balanced stimulus. The movement of an object defined by theta motion is not explicitly encoded in the neuronal activity in areas MT or MST. Our results do not support the hypothesis that the neuronal activity in these areas codes for the direction of stimulus movement independent of specific stimulus parameters. Furthermore, our results emphasize the relevance of different segmentation cues between figure and background. Therefore the notion that there are multiple sites responsible for the processing of second-order motion is strongly supported.

Effect of chromatic flicker on circulation of the optic nerve

To determine the response of human optic nerve head (ONH) blood flow (delta F) to heterochromatic equiluminant flicker modulation (eql-fl) and compare it to the response induced by pure luminance flicker (l-fl). In 5 normal volunteers the ONH blood flow was measured by conventional laser Doppler flowmetry. Stimuli were generated by green and red light emitting diodes and delivered to the eye through a fundus camera illumination optic. Both green and red illuminances were square wave modulated in counter phase at different frequencies between 2 and 40 Hz. delta F was defined as the ratio between the ONH blood flow after 1 min stimulation and a baseline blood flow measured prior to the stimulation. In response to a 2 Hz eql-fl, ONH blood flow increases by 36% in average. delta F versus flicker frequency displayed the characteristics of a low-pass function with a cutoff frequency of 10 Hz for an eql-fl and a band-pass function with broad maximum around 10 Hz for the I-fl. delta F in human ONH can be evoked by heterochromatic equiluminant flicker modulation. The blood flow frequency response to eql-fl and I-fl are similar to the neural activity dominated by the Parvo- and Magno-cellular activity, respectively. These findings offer a new approach to study the neurovascular coupling at the ONH in both physiological and diseased conditions involving predominantly or selectively the Magno- and Parvo-pathways.

Luminance flicker sensitivity in positive- and negative-symptom schizophrenia.

The aim of the present research was to investigate magnocellular and parvocellular channel disorders using luminance-flicker sensitivity in normal observers and a group with schizophrenia. The threshold sensitivity for a sine wave-modulated patch of achromatic flickering light in a gaussian envelope was measured as a function of its temporal frequency (1.0 Hz, 4.0 Hz, 8.0 Hz, 16.0 Hz, 32.0 Hz) and three space average luminance levels (mesopic 3.0 cd/m2, photopic 33.0 cd/m2 and 66.0 cd/m2). The Andreasen scales for the assessment of positive and negative symptoms in schizophrenia were used to classify subjects into subgroups with predominantly positive and negative symptoms. The results showed that there were no significant differences between the control and positive-symptom group in flicker sensitivity as a function of temporal frequency and luminance level, and there were no differences in flicker sensitivity between the three groups at 1.0 Hz at each of the three luminance levels. At 3.0 cd/m2 the negative-symptom group showed significant reductions in flicker sensitivity at 4.0 Hz, 8.0 Hz, 16.0 Hz and 32.0 Hz in comparison with the control and positive-symptom group. At 33.0 cd/m2 the negative-symptom group showed significant reductions in flicker sensitivity at 4.0 Hz and 32.0 Hz, and at 66.0 cd/m2 they showed significant reductions in flicker sensitivity at 4.0 Hz, 8.0 Hz and 32.0 Hz only in comparison with the control. It was concluded that the non-significant differences in flicker sensitivity in the positive-symptom group showed that the processing of temporal information in parvo- and magnocellular channels was unimpaired. Furthermore, the non-significant differences in flicker sensitivity at 1.0 Hz at each of the three luminance levels in the three groups provided evidence that functioning in parvocellular channels was unimpaired in the positive- and negative-symptom group. Finally, it was concluded that the significant reductions in flicker sensitivity at medium and high temporal frequencies in the negative-symptom group provided evidence for an impairment in magnocellular channels.

Interactions between first- and second-order motion revealed by optokinetic nystagmus.

A previous study has suggested that second-order motion is ineffective at driving optokinetic nystagmus (OKN) when presented alone. First- and second-order motion cues interact in creating the perception of motion. Is there an interaction between first- and second-order cues in the control of eye movements? We presented combinations of first- and second-order cues moving in the same or opposite directions and measured the eye movements evoked, to look for a modification of the oculomotor response to first-order motion by simultaneously presented second-order cues. Dynamic random noise was used as a carrier for first- and second-order drifting gratings (13.4 degrees/s; 0.25 cycles/degree; 64 x 48 degrees screen viewed at 28.5 cm). Second-order gratings were defined by spatial modulation of the luminance flicker frequency of noise pixels of constant contrast (50%). A first-order, luminance-defined grating (13.4 degrees/s; 0.25 cycles/degree; variable contrast from 4-50%) was moved in either the same or the opposite direction. Eye movements were recorded by video-oculography from six subjects as they looked straight ahead. The gain (eye velocity/stimulus velocity) of first-order-evoked OKN increased with contrast. The presence of flicker-defined second-order motion in the opposite direction attenuated this OKN below a first-order contrast of 15%, although it had little effect at higher contrasts. When first- and second-order motion were in the same direction, there was an enhancement of the OKN response. We conclude that second-order motion can modify the optokinetic response to simultaneously presented first-order motion.