Eye Tracking Performance Research Articles

A confirmatory factor analysis of components of eye tracking performance

In two eye-tracking studies, we explored whether and how attention to nutrition information mediates consumers’ choice. Consumers had to select either the healthiest option or a product of their preference within an assortment. On each product a particular label (Choices logo, monochrome GDA label, or color-coded GDA label) communicated the product’s nutrient profile. In study 1, participants had to select from 4 products differentiated, in addition to the nutrition information, by flavor (strawberry, muesli, apple, chocolate; varied within participants) and brand (local vs. global, varied between participants). Study 2 further explored brand effect within-participants, and thus only 2 flavors (strawberry, chocolate) were presented within an assortment. Actual choice made, response time and eye movements were recorded. Respondents fixated longer and more often on products with color-coded GDAs label than on products with monochrome GDAs or Choices logo. A health goal resulted in longer and more frequent fixations in comparison to a preference goal. Products with color-coded and monochrome GDAs had the highest likelihood of being chosen, and this effect was related to the attention-getting property of the label (irrespective of brand and flavor effects). The product fixated most had the highest likelihood of being chosen. These results suggest that attention mediates the effect of nutrition labels on choice.

The association between lithium carbonate and smooth pursuit eye tracking among first-episode patients with psychotic affective disorders.

The association between treatment with lithium carbonate and smooth pursuit eye tracking performance was investigated in first-episode patients with psychotic affective disorders. The horizontal pursuit performance of patients with major depression and bipolar disorder who were receiving lithium carbonate was contrasted with that of patients not receiving lithium carbonate. In addition, the accuracy and quality of pursuit eye tracking was examined in bipolar patients whose lithium status changed from the time of initial testing to the time of retest 10 months later. For the combined group of depressed and bipolar patients, treatment with lithium carbonate was not associated with worse pursuit performance. Bipolar disordered patients on lithium did not differ in tracking proficiency from those not on lithium; bipolar patients whose lithium status changed from intake to retest also did not display a significant change in pursuit performance.

Smooth pursuit ocular motor dysfunction in schizophrenia: evidence for a major gene.

Evidence suggests that poor eye tracking relates to genetically transmitted vulnerability for schizophrenia. The authors tested competing models for the genetic transmission of poor eye tracking in a search for major gene effects. Samples from three studies (conducted in Minneapolis, New York, and Vancouver, B.C.) were pooled. Probands (N = 92) were diagnosed as schizophrenic by DSM-III criteria. Of the comparison subjects (N = 171), Vancouver patients were an epidemiologic first-episode group; at other sites unselected admitted patients were studied. First-degree relatives (N = 146) of 65 probands were also studied. Eye tracking was measured while subjects followed a horizontally moving, sinusoidally driven (0.4 Hz) spot of light on a screen. Performance was quantified by root mean square error. Data analysis was by complex segregation analysis (Bonney's class D regressive models). A single major gene is needed to account for poor eye tracking in schizophrenic patients and their relatives. This gene alone can explain about two-thirds of the variance in eye tracking performance. A single gene alone (regardless of dominance) will, however, not account for the data; polygenic factors are also required. Results support postulation of a single gene for ocular motor dysfunction, which may be a risk factor for schizophrenia. Eye tracking may be useful as a gene carrier test in genetic studies of schizophrenia.

Clinical, neuropsychological, and brain structural correlates of smooth-pursuit eye tracking performance in chronic schizophrenia.

Clinical, neuropsychological, and brain structural correlates of smooth-pursuit eye tracking performance in chronic schizophrenia.

Magnetic resonance imaging in schizophrenia: Altered brain morphology associated with P300 abnormalities and eye tracking dysfunction

This study was designed to investigate whether auditory P300 event-related potential and smooth pursuit eye-movement abnormalities in schizophrenia are associated with brain structural changes measured using magnetic resonance imaging (MRI). Serial coronal MRI scans obtained from 31 schizophrenic subjects and 33 volunteer controls were analysed by a rater who had no knowledge of the subjects' diagnoses. The brain areas measured bilaterally were the temporal lobe, hippocampus, amygdala, parahippocampal gyrus, head of caudate, cingulate cortex, frontal cortex, and the lateral ventricles. The areas of the third ventricle, the thickness of the corpus callosum, and the intracranial area were also measured. Auditory P300 and eye tracking performance were recorded on all subjects. There was a significant increase in the latency and a reduction in amplitude of the P300 in the schizophrenic group. Only in the schizophrenic group was P300 latency correlated negatively with the area of the right and left cingulate cortex and positively with the difference in size between the right and left amygdala. In the subgroup of schizophrenic subjects whose P300 latency was greater than 2 standard deviations above the control mean, the area of the left cingulate was significantly smaller than in controls, and the absolute right-left difference in the area of the amygdala was significantly increased. Eye tracking dysfunction in schizophrenia was not related to changes in the amygdala or cingulate cortex but was significantly correlated with enlargments of the lateral ventricles. Schizophrenic subjects with poor eye tracking had significantly larger lateral ventricles than controls. Eye tracking dysfunction, but not P300 abnormality, was correlated with the severity of both positive and negative symptom of schizophrenia. These findings demonstrate that psychopysiological abnormalities are associated with altered brain structure in schizophrenia.

A model of smooth pursuit performance illustrates the relationship between gain, catch-up saccade rate, and catch-up saccade amplitude in normal controls and patients with schizophrenia

Smooth pursuit eye-tracking performance of 37 unmedicated patients with schizophrenia and 45 normal controls was recorded with infrared oculography, and digitized for offline analysis of gain and other measures. Target velocity was 5°/sec. Patients with schizophrenia had significantly lower gain than normal controls, confirming several earlier reports. During low gain smooth pursuit tracking, when eye velocity is slower than target velocity, the saccadic system corrects for the accumulating position error with catch-up saccades (CUS). The rate of CUS and the median CUS amplitude were compared between groups. Patients had significantly more CUS than controls, but the median CUS amplitudes were not significantly different. A nonlinear mathematical model of the relationship between gain, CUS amplitude, and CUS rate during steady-state constant velocity tracking was developed to integrate these findings. According to this model, for a given gain, correction for position error can result from either a few large CUS or many small CUS. The fit of the model to empirical data, as assessed graphically and with linear and nonlinear regression techniques, was excellent. The model fit the data for both patients and controls. The psychiatric eye-tracking literature is discussed from the perspective suggested by the modeled relationship.

Impaired eye tracking performance in patients with presenile onset dementia

Smooth pursuit eye movements, saccades and eye blinks were electrooculographically recorded from 26 healthy subjects of different age and 35 patients with presumptive presenile onset dementia (mean age 54), who had to track a light spot which oscillated with different speeds. Older subjects (mean age 51) performed the eye tracking with less accuracy and more saccades than younger ones (mean age 22). 16 patients with stage CDR 1 according to Washington University Clinical Dementia Rating performed smooth pursuit eye movements significantly worse with increased saccade numbers than the Healthy older subjects and lost attention significantly more often which was measured by omitted trackings to presented target oscillations. Their number of eye blinks was partly increased. The test is found suitable for early diagnosis of dementia onset, supporting clinical findings and presumptive diagnosis by objective parameters.

Clinical, neuropsychological, and brain structural correlates of smooth-pursuit eye tracking performance in chronic schizophrenia.

The relation of smooth-pursuit eye tracking dysfunction to neuropsychological performance, brain structural anomalies, and clinical state was examined in a sample of 61 patients with chronic schizophrenia. No association was found between impaired pursuit oculomotion and measures of chronicity or clinical state. Likewise, no association emerged between eye-tracking integrity and brain structural anomalies. Patients with dysfunctional eye tracking were more likely to have impaired performance on tests that assess frontal lobe functioning. In addition, negative symptoms and a relative absence of positive symptoms. Because negative symptoms are often found among patients with frontal lobe impairment, their association with abnormal eye tracking provides converging support for the hypothesis that the cortical locus of deviant smooth-pursuit eye tracking is in the frontal lobes.

Smooth pursuit eye movements of normal and schizophrenic subjects tracking an unpredictable target

An experimental paradigm employed by several workers in the field of schizophrenic eye movements has involved findingssequences of stimuli that induce saccadic smooth pursuit in the eye movements of normal individuals. It is hoped that the identification of such stimuli will lead to clues concerning the etiology or nature of eye tracking dysfunction in schizophrenia. In this study, the pursuit eye movements of normal and schizophrenic subjects tracking an unpredictable target (composed of summed sine waves) were examined. Eye tracking performance was evaluated both qualitatively and quantitatively using percent root-mean-square (%RMS) error and pursuit gain scores. Schizophrenics are capable of tracking an unpredictable target. This finding has implications for our understanding of schizophrenic information processing during visual tracking.

Eye Tracking Dysfunction is Associated With Partial Trisomy of Chromosome 5 and Schizophrenia: A Response-Reply

In Reply.— Our case study revealed that a proband and his maternal uncle, both of whom had partial trisomy of chromosome 5 and schizophrenia, also had abnormal smooth-pursuit eye tracking. The proband's mother, father, and brother, who had neither any psychiatric disorder nor the partial trisomy, displayed very good eye tracking performance. Although we are pleased that Holzman et al found these data supportive of their latent trait hypothesis, we do not share their reservations and concerns. If we assume that schizophrenia in the proband and uncle arose because they had the chromosomal anomaly, then finding abnormal pursuit tracking in the nonschizophrenic family members would not support the latent trait hypothesis. This family is interesting presumably because the trisomic individuals possess a special genotype (partial trisomy chromosome 5) associated with schizophrenia, while the other members of the family do not. There is, therefore, no reason to expect the nontrisomic, psychiatrically healthy

Eye tracking, schizophrenic symptoms, and schizotypal personality disorder.

Schizophrenic patients and patients with schizotypal personality disorder were significantly more likely than normal controls to demonstrate impaired eye tracking performance. Fifteen of 27 schizophrenics and 15 of 27 schizotypals had impaired eye tracking, compared with 11 of 39 normal controls. In the schizophrenic group, including 10 out-patients in a stable state of relative remission, impaired eye tracking was associated with more severe formal thought disorder and more time spent in psychiatric hospitals. Among stable schizophrenic out-patients, poor eye tracking was related to more severe formal thought disorder and greater overall psychopathology. This pattern of results suggests a possible relation between eye tracking impairment and more severe enduring symptoms across the spectrum of schizophrenic and schizophrenia-related disorders.

The effects of dark adaptation on pursuit tracking dysfunction in psychotics with imparied vestibular suppresion

Smooth pursuit eye tracking performance, evaluated by electronic processing and subjective ratings, was assessed in actively psychotic psychiatric patients and normal controls under conditions of light and dark adaptation and was related to subjects' ability to suppress vestibular nystagmus induced by caloric irrigation. Patients' tracking performance was significantly inferior during the light-adapted condition on all tracking measures. Dark-adaptation eliminated group differences based on electronic analyses, but subjective ratings-which showed a variable relationship to the other tracking measures-did not reflect this improvement. Vestibular nystagmus suppression was significantly impaired in patients relative to controls and this impairment, coupled with smooth pursuit dysfunction and marked improvement in tracking performance during dark-adaptation, suggests that cerebellar dysfunction contributes significantly to tracking dysfunction in psychotic patients.

Pursuit eye movement dysfunctions in schizophrenia. Family evidence for specificity.

In a number of previous investigations, eye tracking dysfunctions had been reliably found in from 50% to 85% of schizophrenic patients, about 40% of manic-depressive patients, and about 8% of the normal population. We report similar smooth pursuit eye movement dysfunctions in 34% of the parents (or 55% of parental pairs) of schizophrenic patients compared with 10% of the parents (or 7% of parental pairs) of manic-depressive patients. Parental eye movement dysfunctions are significantly related to the diagnosis of the patient and not to the patient's eye tracking performance. These data suggest that, in the absence of other CNS disease, these eye tracking dysfunctions represent familial markers of vulnerability to schizophrenia.

Eye tracking impairment: Attentional and psychometric correlates in psychiatric patients

The correlations between eye tracking and a set of attentional and psychometric correlates of psychopathology were studied in groups of schizophrenic, nonschizophrenic psychotic, schizotypal, and neurotic patients (DSM-III criteria), and in a normal control group. Measures of overall and of optimum eye tracking performance were employed. Attentional measures were: reaction time, crossover phenomenon, omission score on the continous performance test, and amplitude of the contingent negative variation. Psychometric measures were: psychoticism, extraversion, and neuroticism. A measure of eye tracking based on the best cycle in the total sequence proved superior to the overall score as a correlate of psychopathology. The correlational patterns differed widely between groups. Most conspicuous were the correlations of eye tracking with psychoticism in psychotics, especially in schizophrenics, and the impressive number of significant correlations with attentional as well as psychometric variables in the schizophrenic category.

Variables affecting eye tracking performance

The effect of age and gender on eye tracking performance was studied in normal healthy subjects. Two measures of tracking performance, phase corrected cross-correlation coefficients and number of catch-up saccades were determined. The cross-correlation measures revealed a differential effect with the elderly men demonstrating significantly better tracking performance than elderly women. An aging effect was found in women and an aging trend in men using the catch-up saccade measure. Other variables influencing tracking performance, in addition to age and sex, were target speed and type of measure. Recognition of this differential effect largely explains the existing controversy as to whether age or sex variables influence tracking performance.

Features that distinguish the smooth-pursuit eye-tracking performance of schizophrenic, affective-disorder, and normal individuals.

Features that distinguish the smooth-pursuit eye-tracking performance of schizophrenic, affective-disorder, and normal individuals.

Features that distinguish the smooth-pursuit eye-tracking performance of schizophrenic, affective-disorder, and normal individuals.

Features that distinguish the smooth-pursuit eye-tracking performance of schizophrenic, affective-disorder, and normal individuals.

Eye tracking in normal twins.

The influence of genetic factors on smooth-pursuit and saccadic eye tracking was determined using 34 pairs of monozygotic and 24 pairs of dizygotic twins. Subjects engaged in smooth-pursuit tracking of different-frequency sinusoidal targets and saccadic tracking of an abruptly moving, rectangular-wave target. Tracking error and phase lag served as dependent measures for the pursuit tasks; saccadic eye tracking performance was evaluated by measuring oculomotor reaction times. The results suggest a genetic basis for smooth-pursuit tracking error; the intraclass correlations for performance averaged over all pursuit tasks were 0.68 and 0.35 for the identical and fraternal twins, respectively. While equivocal results were found for the phase lag data, there was no evidence for the influence of genetic factors on oculomotor response times. These findings are in agreement with the results of twin studies using psychiatric patients.

Two-year retest stability of eye tracking performance and a comparison of electro-oculographic and infrared recording techniques: evidence of EEG in the electro-oculogram.

ABSTRACTThis study assessed the quantitative and qualitative comparability of simultaneously recorded electrooculographic (EOG) and infrared (IR) measures of eye movement and the long‐term retest stability of the EOG. Fifty‐two twins, all of whom performed the same tasks while the EOG was recorded two years ago, engaged in smooth‐pursuit tracking of sinusoidally driven targets ranging in frequency from. 4 to 1.2 Hz and in saccadic tracking of a modified square wave target. In addition to computer‐derived estimates of smooth‐pursuit and saccadic eye tracking proficiency, a measure of saccadic interference during smooth‐pursuit tracking and ratings of the amount of small‐amplitude spiky oscillation in the EOG were made. Two‐year retest stability of these various measures varied from .54 to .83 and were similar to within‐session and one‐week retest reliabilities computed for these same subjects. Correlations between computer‐derived EOG and IR scores ranged from.89 to.99 indicating good correspondence between the two methods. Qualitative EOG‐IR comparability was not high for subjects who showed a pronounced spiky oscillation in the EOG. Spectral analyses of the EOG and concurrently recorded EEG suggest that this spiky rhythm represents EEG (perhaps kappa or alpha), the presence of which is correlated with poor eye tracking.

Metabolic and psychophysiologic studies of cannabidiol-hexobarbital interaction.

Cannabidiol (CBD), 600 mg/day orally for 5 to 12 days, inhibited hexobarbital metabolism in ten subjects. Hexobarbital oral clearance was 36% lower and apparent volume of distribution was 35% smaller, with no change in half-life during CBD. In four subjects who received intravenous and oral hexobarbital, systemic clearance was 36% lower while bioavailability was 10% greater during CBD. Hexobarbital increased fatigue and tremor, impaired eye-tracking performance, and altered the electroencephalogram. Hexobarbital effects were not affected by CBD. Inhibition of metabolism of other drugs should be considered when large amounts of CBD are taken or when CBD is used for therapy.