Alertness Training Increases Visual Processing Speed in Healthy Older Adults.

In this study, we investigated whether alertness training in healthy older adults increases visual processing speed (VPS) and whether functional connectivity in the cingulo-opercular network predicts training gain. Using the theory of visual attention, we derived quantitative estimates of VPS before and after training. In Study 1, 75 healthy older adults participated in alertness training, active-control training, or no training (n = 25 each). A significant Group × Session interaction indicated an increase in VPS in the alertness-training group but not in the control group, despite VPS not differing significantly between groups before training. In Study 2, 29 healthy older adults underwent resting-state functional MRI and then participated in alertness training. Pretraining functional connectivity in the cingulo-opercular network correlated with the individual training-induced change in VPS. In conclusion, results indicate that alertness training improves visual processing in older adults and that functional connectivity in the cingulo-opercular network provides a neural marker for predicting individual training gain.

Neuro-cognitive mechanisms of simultanagnosia in patients with posterior cortical atrophy.

Posterior cortical atrophy is dominated by progressive degradation of parieto-occipital grey and white matter, and represents in most cases a variant of Alzheimer's disease. Patients with posterior cortical atrophy are characterized by increasing higher visual and visuo-spatial impairments. In particular, a key symptom of posterior cortical atrophy is simultanagnosia i.e. the inability to perceive multiple visual objects at the same time. Two neuro-cognitive mechanisms have been suggested to underlie simultanagnosia, either reduced visual short-term memory capacity or decreased visual processing speed possibly resulting from white matter impairments over and above damage to cortical brain areas. To test these distinct hypotheses, we investigated a group of 12 patients suffering from posterior cortical atrophy with homogenous lesion sides in parieto-occipital cortices and varying severity of grey and white matter loss. More specifically, we (i) tested whether impaired short-term memory capacity or processing speed underlie symptoms of simultanagnosia; (ii) assessed the link to grey and white matter damage; and (iii) integrated those findings into a neuro-cognitive model of simultanagnosia in patients with posterior cortical atrophy. To this end, simultaneous perception of multiple visual objects was tested in patients with posterior cortical atrophy mostly with positive Alzheimer's disease biomarkers and healthy age-matched controls. Critical outcome measures were identification of overlapping relative to non-overlapping figures and visuo-spatial performance in tests sensitive to simultanagnosia. Using whole report of briefly presented letter arrays based on the mathematically formulated 'Theory of Visual Attention', we furthermore quantified parameters of visual short-term memory capacity and visual processing speed. Grey and white matter atrophy was assessed by voxel-based morphometry analyses of structural magnetic resonance data. All patients showed severe deficits of simultaneous perception. Compared to controls, we observed a specific slowing of visual processing speed, while visual short-term memory capacity was preserved. In a regression analysis, processing speed was identified as the only significant predictor of simultaneous perception deficits that explained a high degree of variance (70-82%) across simultanagnosia tasks. More severe slowing was also indicative for more severe impairments in reading and scene comprehension. Voxel-based morphometry yielded extensive reductions of grey and white matter in parieto-occipital and thalamic brain areas. Importantly, the degree of individual atrophy of white matter in left superior parietal lobe, but not of any grey matter region, was associated with processing speed. Based on these findings, we propose that atrophy of white matter commonly observed in posterior cortical atrophy leads to slowing of visual processing speed, which underlies the overt clinical symptoms of simultanagnosia.

Visual attention in preterm born adults: specifically impaired attentional sub-mechanisms that link with altered intrinsic brain networks in a compensation-like mode.

Although pronounced and lasting deficits in selective attention have been observed for preterm born individuals it is unknown which specific attentional sub-mechanisms are affected and how they relate to brain networks. We used the computationally specified 'Theory of Visual Attention' together with whole- and partial-report paradigms to compare attentional sub-mechanisms of pre- (n=33) and full-term (n=32) born adults. Resting-state fMRI was used to evaluate both between-group differences and inter-individual variance in changed functional connectivity of intrinsic brain networks relevant for visual attention. In preterm born adults, we found specific impairments of visual short-term memory (vSTM) storage capacity while other sub-mechanisms such as processing speed or attentional weighting were unchanged. Furthermore, changed functional connectivity was found in unimodal visual and supramodal attention-related intrinsic networks. Among preterm born adults, the individual pattern of changed connectivity in occipital and parietal cortices was systematically associated with vSTM in such a way that the more distinct the connectivity differences, the better the preterm adults' storage capacity. These findings provide first evidence for selectively changed attentional sub-mechanisms in preterm born adults and their relation to altered intrinsic brain networks. In particular, data suggest that cortical changes in intrinsic functional connectivity may compensate adverse developmental consequences of prematurity on visual short-term storage capacity.

The capacity of attention and simultaneous perception of objects: a group study of Huntington's disease patients.

Using a whole report-paradigm based on [Bundesen, C. (1990). A theory of visual attention. Psychological Review, 97, 523-547; Bundesen, C. (1998). A computational theory of visual attention. Philosophical Transactions of the Royal Society of London B, Biological Sciences, 353, 1271-1281] theory of visual attention (TVA), [Finke, K., Bublak, P., Dose, M., Müller, H. J., & Schneider, W. X. (2006). Parameter-based assessment of spatial and non-spatial attentional deficits in Huntington's disease. Brain, 129, 1137-1151] demonstrated profound reductions in perceptual processing speed and visual working memory (WM) storage capacity in Huntington's disease (HD) patients. A comparably severe impairment of visual processing capacity has previously been reported for two simultanagnosia patients [Duncan, J., Bundesen, C., Olson, A., Humphreys, G., Ward, R., Kyllingsbaek, S., van Raamsdonk, M., Rorden, C., & Chavda, S. (2003). Attentional functions in dorsal and ventral simultanagnosia. Cognitive Neuropsychology, 20, 675-702]. To investigate whether such a deficit does also prevail in HD, the simultaneous perception of visual objects was tested in 10 HD patients under free viewing conditions and without time constraints. Objects were presented under four different conditions: (i) single, (ii) multiple adjacent, (iii) multiple embedded, and (iv) multiple overlapping. The dependent measure was the percentage of identification failures. Performance was compared to that of 15 healthy subjects matched for age, education, gender and general mental ability. For HD patients, the percentage of errors in the various testing conditions was examined for correlations with the TVA parameters of visuo-perceptual processing speed and WM storage capacity. These parameters were estimated using verbal whole report of briefly presented letters. TVA permits the two parameters to be estimated mathematically independently and relatively unaffected by any motor deficits present in HD. The identification error rate was substantially increased in HD patients, compared to control subjects, in the overlapping-figures subtest. This deficit was significantly and negatively correlated with processing speed, whereas there was no correlation with WM storage capacity. These results demonstrate the presence of deficits in simultaneous perception in HD, related to a severe reduction in perceptual processing speed. The results are discussed with respect to a dopamine mediated decline of cortical cholinergic activation, diminishing the number of visual objects that can be simultaneously represented within the visual processing system.

Simultaneous object perception deficits are related to reduced visual processing speed in amnestic mild cognitive impairment.

Simultanagnosia, an impairment in simultaneous object perception, has been attributed to deficits in visual attention and, specifically, to processing speed. Increasing visual attention deficits manifest over the course of Alzheimer's disease (AD), where the first changes are present already in its symptomatic predementia phase: amnestic mild cognitive impairment (aMCI). In this study, we examined whether patients with aMCI due to AD show simultaneous object perception deficits and whether and how these deficits relate to visual attention. Sixteen AD patients with aMCI and 16 age-, gender-, and education-matched healthy controls were assessed with a simultaneous perception task, with shapes presented in an adjacent, embedded, or overlapping manner, under free viewing without temporal constraints. We used a parametric assessment of visual attention based on the Theory of Visual Attention. Results show that patients make significantly more errors than controls when identifying overlapping shapes, which correlate with reduced processing speed. Our findings suggest simultaneous object perception deficits in very early AD, and a visual processing speed reduction underlying these deficits.

Spatial and non-spatial attention deficits in neurodegenerative diseases: assessment based on Bundesen's theory of visual attention (TVA).

PURPOSE: The aim was to present evidence that, similarly as in neglect, a combined pattern of spatial and non-spatial deficits of visual attention can also be typically observed in patients suffering from neurodegenerative disorders. METHOD: Whole and partial report of brief letter arrays, based on Bundesen's 'theory of visual attention' (TVA), was applied in patients suffering from Huntington's disease (HD), mild cognitive impairment (MCI), or Alzheimer's disease (AD). TVA-based parameter estimates were derived reflecting (a) perceptual processing speed and visual working memory storage capacity as non-spatial aspects of visual attention (determined by whole report performance), and (b) spatial attentional weighting (determined by partial report performance). RESULTS: Processing speed was severely slowed in HD, and also reduced, although to a lesser degree, in MCI and AD patients. In HD and AD patients, but not in MCI patients, a strong leftward bias of spatial attention was observed. CONCLUSION: Neglect and neurodegenerative diseases both involve a similar constellation of non-spatial and spatial deficits of visual attention. Therefore, by using TVA-based measurement, results from both fields of research may fruitfully inform each other in future studies, thus improving our understanding of the interaction of spatial and non-spatial attention deficits and its behavioral consequences.

Video game experience and its influence on visual attention parameters: an investigation using the framework of the Theory of Visual Attention (TVA).

Experts with video game experience, in contrast to non-experienced persons, are superior in multiple domains of visual attention. However, it is an open question which basic aspects of attention underlie this superiority. We approached this question using the framework of Theory of Visual Attention (TVA) with tools that allowed us to assess various parameters that are related to different visual attention aspects (e.g., perception threshold, processing speed, visual short-term memory storage capacity, top-down control, spatial distribution of attention) and that are measurable on the same experimental basis. In Experiment 1, we found advantages of video game experts in perception threshold and visual processing speed; the latter being restricted to the lower positions of the used computer display. The observed advantages were not significantly moderated by general person-related characteristics such as personality traits, sensation seeking, intelligence, social anxiety, or health status. Experiment 2 tested a potential causal link between the expert advantages and video game practice with an intervention protocol. It found no effects of action video gaming on perception threshold, visual short-term memory storage capacity, iconic memory storage, top-down control, and spatial distribution of attention after 15 days of training. However, observations of a selected improvement of processing speed at the lower positions of the computer screen after video game training and of retest effects are suggestive for limited possibilities to improve basic aspects of visual attention (TVA) with practice.

Asymmetric loss of parietal activity causes spatial bias in prodromal and mild Alzheimer's disease.

BACKGROUND: In Alzheimer's disease (AD), loss of effective neuronal activity is reflected by cortical glucose hypometabolism. Hypometabolism in the posterior parietal cortex (PPC) is among the first in vivo signs of AD; however, its functional impact on large-scale brain mechanisms and behavior is poorly understood. The lateral PPC contributes to spatial attention constituting a basic function of the human brain. We hypothesized 1) that lateral PPC hypometabolism is associated with impaired spatial attention in very early AD and 2) that impaired competition of effective neuronal activity across hemispheres might underlie this deficit in terms of brain mechanisms. METHODS: A model-based imaging approach was applied to assess patients with prodromal (n = 28) and mild (n = 7) AD. Quantitative attention parameters, derived from performance on simple psychophysical tasks and analyzed by Bundesen's computational theory of visual attention, were related to brain metabolism, measured by (18)F-fluorodeoxyglucose positron emission tomography. RESULTS: Patients' left and right lateral PPC metabolism was reduced. Nine patients had significant spatial attentional bias on the left side and two patients on the right. Direction and degree of spatial bias was correlated with direction and degree of an interhemispheric metabolism bias in the inferior parietal lobe and temporoparietal junction. CONCLUSIONS: Our data provide evidence that in very early AD, asymmetric hypometabolism of the lateral PPC causes spatial attentional bias. Results are broadly consistent with the model that asymmetrically impaired effective neuronal PPC activity in AD biases the competition of visual objects for cortical representation and access to awareness to one side.

Staged decline of visual processing capacity in mild cognitive impairment and Alzheimer's disease.

Visual information intake was assessed with a whole-report task in patients with probable Alzheimer's disease (AD), mild cognitive impairment (MCI), and healthy elderly control subjects. Based on a theory of visual attention (TVA), four parameters were derived characterising different aspects of visual processing capacity: perceptual threshold, iconic memory, processing speed, and visual short-term memory (VSTM) storage capacity. Results indicated increased perceptual thresholds in MCI, and an additional decline in processing speed and VSTM storage capacity in AD. Cholinomimetic medication had beneficial effects on processing speed in AD patients. Perceptual thresholds were associated with disease duration, but not with cognitive measures, while the reverse was true for speed and VSTM measures. These results reveal a staged pattern of deficits affecting pre-attentive visual processing in MCI, and attentive processing in AD. It is compatible with the amyloid cascade hypothesis and suggests that impaired visual processing is a pathological feature present already at the MCI stage and might represent a distinct marker of upcoming AD independently from memory deficits.