Role of the Dorsal Posterior Parietal Cortex in the Accurate Perception of Object Magnitude in Peripheral Vision

Following superior parietal lobule and intraparietal sulcus (SPL-IPS) damage, optic ataxia patients underestimate the distance of objects in the ataxic visual field such that they produce hypometric pointing errors. The metrics of these pointing errors relative to visual target eccentricity fit the cortical magnification of central vision. The SPL-IPS would therefore implement an active “peripheral magnification” to match the real metrics of the environment for accurate action. We further hypothesized that this active compensation of the central magnification by the SPL-IPS contributes to actual object’ size perception in peripheral vision. Three optic ataxia patients and 10 age-matched controls were assessed in comparing the thickness of two rectangles flashed simultaneously, one in central and another in peripheral vision. The bilateral optic ataxia patient exhibited exaggerated underestimation bias and uncertainty compared to the control group in both visual fields. The two unilateral optic ataxia patients exhibited a pathological asymmetry between visual fields: size perception performance was affected in their contralesional peripheral visual field compared to their healthy side. These results demonstrate that the SPL-IPS contributes to accurate size perception in peripheral vision.

Reconsidering the role of attention in optic ataxia: A case report of optic ataxia in visual neglect and extinction

Optic ataxia is a rare condition following dorsal visual stream lesions characterized by peripheral misreaching. This ‘pure’ visuomotor condition is claimed to be dissociable from attentional disorders, such as visual neglect and extinction. However, the relationship between optic ataxia, neglect and extinction is still controversial and recently it has even been suggested these conditions have a common attentional cause. In this single-case report, we investigated 67-year-old female patient E.B. with left visual neglect and extinction following right temporo-parietal and frontal strokes. Unlike most neglect patients, E.B. did not present left hemiparesis or left homonymous hemianopia. This unusual presentation allowed us to study, for the first time, the impact of left visual attentional disorders on reaching with both arms in both free and peripheral vision conditions. Specifically, we assessed whether patient E.B. would present the classic peripheral misreaching deficits reported in patients with optic ataxia. We found that patient E.B.’s reaching accuracy was significantly impaired, when compared to a gender and age-matched control sample (N=11), only in peripheral vision and only for targets presented in her neglected field, regardless of the hand used. Her performance was comparable to controls in free vision for both arms. This demonstrates that a patient with visual neglect and extinction also presents an ataxic field, a deficit typically described as optic ataxia. Our findings suggest that, at least in peripheral vision, attention and visuomotor deficits may be related which challenges long-standing claims of a dissociation between attentional disorders and optic ataxia.

When Mechanical Computations Explain Better

In this paper I defend the epistemic value of the representational-computational view of cognition by arguing that it has explanatory merits that cannot be ignored. To this end, I focus on the virtue of a computational explanation of optic ataxia, a disorder characterized by difficulties in executing visually-guided reaching tasks, although ataxic patients do not exhibit any specific disease of the muscular apparatus. I argue that addressing cases of patients who are suffering from optic ataxia by invoking a causal role for internal representations is more effective than merely relying on correlations between bodily and environmental variables. This argument has consequences for the epistemic assessment of radical enactivism, whichRE invokes the Dynamical System Theory as the best tool for explaining cognitive phenomena.

Corticobasal syndrome with Balint syndrome: a clue for Alzheimer disease pathology

Context: Balint syndrome (BS), first described in 1909, has three core features: optic ataxia, oculomotor apraxia and simultanagnosia, and has been described after various conditions amongst vascular, infectious, demyelinating and degenerative diseases1 . It has already been reported concomitant with corticobasal syndrome (CBS)2 . Case report: 59 year-old male without history of previous diseases presented with behavior changes in the last two years. He had a previous diagnosis of “stroke” because frequent falls to the left side and difficulty in using his left hand for simple daily activities. After that, he gradually evolved with visual problems (bumped into objects inside his house), fear of walking or sitting, and required constant assistance for basic activities of daily living. On physical examination he presented with clear visuospatial dysfunction, characterized by simultanagnosia, oculomotor apraxia and optic ataxia. Bilateral asymmetric upper limb apraxia (worse on left side), dystonic posturing and stimulus-sensitive myoclonus in the left arm were also present. No signs of parkinsonism or language/speech disturbances were identified. Brain MRI showed severe asymmetric biparietal lobe atrophy (right more than left). DISCUSSION: The pathologic findings underlying CBS are variable, including Corticobasal Degeneration, Progressive Supranuclear Palsy, Frontotemporal Lobar Degeneration and Alzheimer Disease (AD). The association of BS and CBS favors the possibility of AD pathologic findings3 . Imaging methods like FDG-PET have recently been shown to be capable of distinguishing AD-related CBS from those associated with other pathologies4 . FDG-PET is not widely available in our country; than the presence of BS in CBS patients may individualize their treatment.

Visually guided reaching in Alzheimer's disease and mild cognitive impairment

Recent evidence has implicated areas within the posterior parietal cortex (PPC), as among the first to show pathophysiological changes in Alzheimer’s disease. Focal brain damage to the PPC can cause optic ataxia, a specific deficit in reaching to peripheral targets. Visuomotor deficits in optic ataxia are often only detected when reaching to objects in peripheral vision, therefore this condition can often go unnoticed. The present study investigated whether peripheral misreaching is a feature of Alzheimer’s disease. Reaching ability was assessed in individuals with a clinical diagnosis of mild-to-moderate Alzheimer’s and mild cognitive impairment (MCI), compared to a control group of healthy, older adults. Participants were required to reach to targets presented in central vision or in the periphery using two reaching tasks; one in the lateral plane and another presented in radial depth. Case-control comparisons identified 1/10 MCI and 3/17 Alzheimer’s patients with severe peripheral reaching deficits at the individual level, but group-level comparisons did not find significantly higher peripheral reaching error in neither Alzheimer’s nor MCI groups. However, exploratory analyses showed significantly increased reach duration in both Alzheimer’s and MCI groups relative to controls. We conclude that Alzheimer’s disease may lead to a visuomotor impairment that is compensated for by a slowing down of the reach movement to maintain accuracy. However, these findings suggest that peripheral reaching deficits similar to what is observed in optic ataxia are unlikely to be a common feature of Alzheimer’s disease.