Chronic visual neglect prevents brain-damaged patients from returning to an independent and active life. Detecting predictors of persistent neglect as early as possible after the stroke is therefore crucial to plan the relevant interventions. Neglect signs do not only depend on focal brain lesions, but also on dysfunction of large-scale brain networks connected by white matter bundles. We explored the relationship between markers of axonal degeneration occurring after the stroke and visual neglect chronicity. A group of 45 patients with unilateral strokes in the right hemisphere underwent cognitive testing for neglect twice, first at the subacute phase (<3 months after onset) and then at the chronic phase (>1 year). For each patient, magnetic resonance imaging including diffusion sequences was performed at least 4 months after the stroke. After masking each patient's lesion, we used tract-based spatial statistics to obtain a voxel-wise statistical analysis of the fractional anisotropy data. Twenty-seven patients had signs of visual neglect at initial testing. Only 10 of these patients had recovered from neglect at follow-up. When compared with patients without neglect, the group including all subacute neglect patients had decreased fractional anisotropy in the second (II) and third (III) branches of the right superior longitudinal fasciculus, as well as in the splenium of the corpus callosum. The subgroup of chronic patients showed reduced fractional anisotropy in a portion the splenium, the forceps major, which provides interhemispheric communication between regions of the occipital lobe and of the superior parietal lobules. The severity of neglect correlated with fractional anisotropy values in superior longitudinal fasciculus II/III for subacute patients and in its caudal portion for chronic patients. Our results confirm a key role of fronto-parietal disconnection in the emergence and chronic persistence of neglect, and demonstrate an implication of caudal interhemispheric disconnection in chronic neglect. Splenial disconnection may prevent fronto-parietal networks in the left hemisphere from resolving the activity imbalance with their right hemisphere counterparts, thus leading to persistent neglect.

Unilateral spatial neglect (USN) is a neurological disorder often observed following damage to the right cerebral hemisphere. Patients with USN are no longer able to take into account stimuli presented on the left side of space. In this article, we will discuss the neuroanatomical correlates that underlie visuospatial attention and can cause USN, an area of growing research interest in the past 20 years. This syndrome has often been related to cortical damage, notably in the inferior parietal lobule. Other data have also implicated lesions in the inferior frontal gyrus or the superior temporal gyrus. In this article, we will highlight the relevance of viewing USN as a disconnection syndrome of interconnected cerebral areas, as opposed to a focal cortical syndrome. We will review data that provide evidence of intrahemispheric disconnection, in particular within the right hemisphere's frontoparietal networks connected by the superior longitudinal fasciculus. Recent findings suggest that interhemispheric disconnection could also contribute to the manifestations of USN. Most importantly, interhemispheric disconnection might be a predictive factor for the chronicity of this disorder. This hypothesis implies that the left hemisphere by itself is not able to compensate for the patients' deficits. Recovery requires the ability to exchange information between the two hemispheres, particularly in the posterior parietal and occipital regions.

Prism adaptation (PA) is responsible for an expansion of sensori-motor after-effects to cognitive domains for patients with spatial neglect. One important question is whether the cognitive after-effects induced by PA may also concern higher aspects of spatial cognition, such as navigation and topographic memory, which are critical in everyday life. The aim of this study was to assess whether multiple sessions of right PA can affect navigation and topographic memory. Seven right brain-damaged (RBD) patients with chronic neglect were included. We used a virtual supermarket named VAP-S which is an original paradigm, similar to the “shopping list test” during which patients had to purchase items from a list of eight products. Furthermore, in order to assess generalization of PA effects on constructing a spatial map from virtual information, each participant was then asked to draw the map of the virtual supermarket from memory. Regarding navigation performance, significant results were obtained: session duration reduction, fewer numbers of pauses and omissions, more items purchased on the left side and more items purchased over all. A long-lasting effect was noted, up to one month after PA. The representational task performance was also significantly increased for map drawing, with a reduction of the right shift of the symmetry axis of the map, more items drawn on the left side of maps and over all, and more items correctly located on the map. Some of these effects lasted for at least 7 days. These results suggest an expansion of PA benefit to a virtual environment. Crucially, the cognitive benefits induced by PA were noted for complex spatial cognition tasks required in everyday life such as navigation and topographic memory and this improvement was maintained for up to 1 month.

Visual neglect is a frequent and disabling consequence of right hemisphere damage. Previous work demonstrated a probable role of posterior callosal dysfunction in the chronic persistence of neglect signs. Prism adaptation is a non-invasive and convenient technique to rehabilitate chronic visual neglect, but it is not effective in all patients. Here we aimed to assess the hypothesis that prism adaptation improves left neglect by facilitating compensation through the contribution of the left, undamaged hemisphere. We assessed the relationship between prism adaptation effects, cortical thickness and white matter integrity in a group of 14 patients with unilateral right-hemisphere strokes and chronic visual neglect. Results showed that patients who benefitted from prism adaptation had thicker cortex in temporo-parietal, prefrontal and cingulate areas of the left, undamaged hemisphere. Additionally, these patients had a higher fractional anisotropy value in the body and genu of the corpus callosum. Results from normal controls show that these callosal regions connect temporo-parietal, sensorimotor and prefrontal areas. Finally, shorter time intervals from the stroke tended to improve patients' response to prism adaptation. We concluded that prism adaptation may improve left visual neglect by promoting the contribution of the left hemisphere to neglect compensation. These results support current hypotheses on the role of the healthy hemisphere in the compensation for stroke-induced, chronic neuropsychological deficits, and suggest that prism adaptation can foster this role by exploiting sensorimotor/prefrontal circuits, especially when applied at early stages post-stroke.

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PA involves persistent reduction in postural asymmetry in RBD patients without neglect. These findings were obtained at a chronic stage. This new effect cannot be explained by reduction in spatial attentional shift. Improvement may be explained by a better calibration of extra personal space frames used for posture, without effect on personal space frame. Findings argue in favour of a bottom-up effect of PA on mechanisms underlying spatial cognition.

Visual neglect is a frequent and disabling consequence of right hemisphere damage. Previous evidence demonstrated a probable role of posterior callosal dysfunction in the chronic persistence of neglect signs. Prism adaptation is a non-invasive and convenient technique to rehabilitate chronic visual neglect, but it is not effective in all patients. Here we hypothesized that prism adaptation improves left neglect by facilitating compensation through the contribution of the left, undamaged hemisphere. To test this hypothesis, we assessed the relationship between prism adaptation effects, cortical thickness and white matter integrity in a group of 14 patients with unilateral right-hemisphere strokes and chronic visual neglect. Consistent with our hypothesis, patients who benefitted from prism adaptation had a thicker cortex in temporo-parietal, prefrontal and cingulate areas of the left, undamaged hemisphere.Additionally, these patients had higher microstructural integrity of the body and genu of the corpus callosum. These callosal regions connect temporo-parietal, sensorimotor and prefrontal areas. Thus, prism adaptation may ameliorate signs of left visual neglect by promoting the contribution of the left hemisphere to neglect compensation. These results support current hypotheses on the role of the healthy hemisphere in the compensation for stroke-induced, chronic neuropsychological deficits, and suggest that prism adaptation can foster this role by exploiting sensorimotor/prefrontal circuits for neglect compensation. Highlights:• Visual neglect is a disabling condition resulting from right hemisphere damage • Prism adaptation is a promising therapy, but not all patients respond • We assessed the anatomical predictors of patients' response to prism adaptation • Study of cortical thickness and white matter integrity • Importance of fronto-parietal networks in the left, healthy hemisphere for recovery • Importance of callosal connections in the genu and body for recovery