Motion blur and motion sharpening in the human visual system

AbstractThe effect of motion sharpening upon blur discrimination thresholds was examined for a range of speeds and blur widths. Blur discrimination thresholds were measured for drifting edges whose blur was either physically or perceptually constant. Under conditions where edges were kept at a constant physical blur width, discrimination thresholds rose as a function of speed as previously reported. However, when the perceived blur of edges was held constant, discrimination performance was more-or-less constant for speeds up to at least 6.3 deg sec−1. The results indicate that the deterioration of blur discrimination performance with speed may be due to motion sharpening and not motion blur as has previously been suggested. The results are discussed in terms of a scheme whereby a non-linearity in motion processing serves to sharpen moving edges, whilst the finite integration time of the system tends to smear them

The effect of contrast adaptation on briefly presented stimuli

AbstractWilson and Humanski (1993) have recently reported evidence that adapting to low temporal frequency sinewave gratings yields little threshold elevation for briefly presented test stimuli. We postulated that brief stimuli may be detected by a transient channel which would be minimally affected by a low temporal frequency adapting pattern. We therefore measured the effect of adaptation om briefly presented test stimuli for a wider range of adapting temporal frequencies. The results indicate that adaptation may yield threshold elevation for briefly presented stimuli and that threshold elevation is greater for high than low temporal frequency adapting patterns. These results are consistent with the hypothesis that briefly presented stimuli are detected by a transient channel

Motion sharpening and contrast: Gain control precedes compressive non-linearity?

AbstractBlurred edges appear sharper in motion than when they are stationary. We (Vision Research 38 (1998) 2108) have previously shown how such distortions in perceived edge blur may be accounted for by a model which assumes that luminance contrast is encoded by a local contrast transducer whose response becomes progressively more compressive as speed increases. If the form of the transducer is fixed (independent of contrast) for a given speed, then a strong prediction of the model is that motion sharpening should increase with increasing contrast. We measured the sharpening of periodic patterns over a large range of contrasts, blur widths and speeds. The results indicate that whilst sharpening increases with speed it is practically invariant with contrast. The contrast invariance of motion sharpening is not explained by an early, static compressive non-linearity alone. However, several alternative explanations are also inconsistent with these results. We show that if a dynamic contrast gain control precedes the static non-linear transducer then motion sharpening, its speed dependence, and its invariance with contrast, can be predicted with reasonable accuracy

Motion, flash, and flicker:A unified spatiotemporal model of perceived edge sharpening

Blurred edges appear sharper in motion than when they are stationary. We proposed a model of this motion sharpening that invokes a local, nonlinear contrast transducer function (Hammett et al, 1998 Vision Research 38 2099-2108). Response saturation in the transducer compresses or 'clips' the input spatial waveform, rendering the edges as sharper. To explain the increasing distortion of drifting edges at higher speeds, the degree of nonlinearity must increase with speed or temporal frequency. A dynamic contrast gain control before the transducer can account for both the speed dependence and approximate contrast invariance of motion sharpening (Hammett et al, 2003 Vision Research, in press). We show here that this model also predicts perceived sharpening of briefly flashed and flickering edges, and we show that the model can account fairly well for experimental data from all three modes of presentation (motion, flash, and flicker). At moderate durations and lower temporal frequencies the gain control attenuates the input signal, thus protecting it from later compression by the transducer. The gain control is somewhat sluggish, and so it suffers both a slow onset, and loss of power at high temporal frequencies. Consequently, brief presentations and high temporal frequencies of drift and flicker are less protected from distortion, and show greater perceptual sharpening

A primary care, multi-disciplinary disease management program for opioid-treated patients with chronic non-cancer pain and a high burden of psychiatric comorbidity

BACKGROUND: Chronic non-cancer pain is a common problem that is often accompanied by psychiatric comorbidity and disability. The effectiveness of a multi-disciplinary pain management program was tested in a 3 month before and after trial. METHODS: Providers in an academic general medicine clinic referred patients with chronic non-cancer pain for participation in a program that combined the skills of internists, clinical pharmacists, and a psychiatrist. Patients were either receiving opioids or being considered for opioid therapy. The intervention consisted of structured clinical assessments, monthly follow-up, pain contracts, medication titration, and psychiatric consultation. Pain, mood, and function were assessed at baseline and 3 months using the Brief Pain Inventory (BPI), the Center for Epidemiological Studies-Depression Scale scale (CESD) and the Pain Disability Index (PDI). Patients were monitored for substance misuse. RESULTS: Eighty-five patients were enrolled. Mean age was 51 years, 60% were male, 78% were Caucasian, and 93% were receiving opioids. Baseline average pain was 6.5 on an 11 point scale. The average CESD score was 24.0, and the mean PDI score was 47.0. Sixty-three patients (73%) completed 3 month follow-up. Fifteen withdrew from the program after identification of substance misuse. Among those completing 3 month follow-up, the average pain score improved to 5.5 (p = 0.003). The mean PDI score improved to 39.3 (p < 0.001). Mean CESD score was reduced to 18.0 (p < 0.001), and the proportion of depressed patients fell from 79% to 54% (p = 0.003). Substance misuse was identified in 27 patients (32%). CONCLUSIONS: A primary care disease management program improved pain, depression, and disability scores over three months in a cohort of opioid-treated patients with chronic non-cancer pain. Substance misuse and depression were common, and many patients who had substance misuse identified left the program when they were no longer prescribed opioids. Effective care of patients with chronic pain should include rigorous assessment and treatment of these comorbid disorders and intensive efforts to insure follow up

GABA predicts visual intelligence

AbstractEarly psychological researchers proposed a link between intelligence and low-level perceptual performance. It was recently suggested that this link is driven by individual variations in the ability to suppress irrelevant information, evidenced by the observation of strong correlations between perceptual surround suppression and cognitive performance. However, the neural mechanisms underlying such a link remain unclear. A candidate mechanism is neural inhibition by gamma-aminobutyric acid (GABA), but direct experimental support for GABA-mediated inhibition underlying suppression is inconsistent. Here we report evidence consistent with a global suppressive mechanism involving GABA underlying the link between sensory performance and intelligence. We measured visual cortical GABA concentration, visuo-spatial intelligence and visual surround suppression in a group of healthy adults. Levels of GABA were strongly predictive of both intelligence and surround suppression, with higher levels of intelligence associated with higher levels of GABA and stronger surround suppression. These results indicate that GABA-mediated neural inhibition may be a key factor determining cognitive performance and suggests a physiological mechanism linking surround suppression and intelligence

Evacetrapib and Cardiovascular Outcomes in High-Risk Vascular Disease

BACKGROUND: The cholesteryl ester transfer protein inhibitor evacetrapib substantially raises the high-density lipoprotein (HDL) cholesterol level, reduces the low-density lipoprotein (LDL) cholesterol level, and enhances cellular cholesterol efflux capacity. We sought to determine the effect of evacetrapib on major adverse cardiovascular outcomes in patients with high-risk vascular disease. METHODS: In a multicenter, randomized, double-blind, placebo-controlled phase 3 trial, we enrolled 12,092 patients who had at least one of the following conditions: an acute coronary syndrome within the previous 30 to 365 days, cerebrovascular atherosclerotic disease, peripheral vascular arterial disease, or diabetes mellitus with coronary artery disease. Patients were randomly assigned to receive either evacetrapib at a dose of 130 mg or matching placebo, administered daily, in addition to standard medical therapy. The primary efficacy end point was the first occurrence of any component of the composite of death from cardiovascular causes, myocardial infarction, stroke, coronary revascularization, or hospitalization for unstable angina. RESULTS: At 3 months, a 31.1% decrease in the mean LDL cholesterol level was observed with evacetrapib versus a 6.0% increase with placebo, and a 133.2% increase in the mean HDL cholesterol level was seen with evacetrapib versus a 1.6% increase with placebo. After 1363 of the planned 1670 primary end-point events had occurred, the data and safety monitoring board recommended that the trial be terminated early because of a lack of efficacy. After a median of 26 months of evacetrapib or placebo, a primary end-point event occurred in 12.9% of the patients in the evacetrapib group and in 12.8% of those in the placebo group (hazard ratio, 1.01; 95% confidence interval, 0.91 to 1.11; P=0.91). CONCLUSIONS: Although the cholesteryl ester transfer protein inhibitor evacetrapib had favorable effects on established lipid biomarkers, treatment with evacetrapib did not result in a lower rate of cardiovascular events than placebo among patients with high-risk vascular disease. (Funded by Eli Lilly; ACCELERATE ClinicalTrials.gov number, NCT01687998 .)