Spatial neglect is a perplexing neuropsychological syndrome, in which patients fail to detect (and/or respond to) stimuli located contralaterally to their (most often right) hemispheric lesion. Neglect is characterized by a wide heterogeneity, and a role for multiple components has been suggested, but the exact nature of the critical components remains unclear. Moreover, many different lesion sites have been reported, leading to enduring controversies about the relative contribution of different cortical and/or subcortical brain regions. Here we report a systematic anatomo-functional study of 80 patients with a focal right hemisphere stroke, who were examined by a series of neuropsychological tests assessing different clinical manifestations of neglect. We first performed a statistical factorial analysis of their behavioural performance across all tests, in order to break down neglect symptoms into coherent profiles of co-varying deficits. We then examined the neural correlates of these distinct neglect profiles using a statistical voxel-based lesion-symptom mapping method that correlated the anatomical extent of brain damage with the relative severity of deficits along the different profiles in each patient. Our factorial analysis revealed three main factors explaining 82% of the total variance across all neglect tests, which suggested distinct components related to perceptive/visuo-spatial, exploratory/visuo-motor, and allocentric/object-centred aspects of spatial neglect. Our anatomical voxel-based lesion-symptom mapping analysis pointed to specific neural correlates for each of these components, including the right inferior parietal lobule for the perceptive/visuo-spatial component, the right dorsolateral prefrontal cortex for the exploratory/visuo-motor component, and deep temporal lobe regions for the allocentric/object-centred component. By contrast, standard anatomical overlap analysis indicated that subcortical damage to paraventricular white matter tracts was associated with severe neglect encompassing several tests. Taken together, our results provide new support to the view that the clinical manifestations of hemispatial neglect might reflect a combination of distinct components affecting different domains of spatial cognition, and that intra-hemispheric disconnection due to white matter lesions might produce severe neglect by impacting on more than one functional domain.

SCD patients in Cameroon presented a very high prevalence of cognitive deficits, with a specific impairment of executive functions and attention. Routine neuropsychological evaluation for early detection of cognitive deficits in SCD patients could represent a cost-effective tool to implement in resource-limited contexts such as in sub-Saharan Africa.

Sir,We would like to make a few comments on the interesting paper recently published in Brain by Karnath et al. (2011). We were impressed by the careful assessment of spatial neglect during acute and chronic phase, which was combined with a solid voxel-wise lesion symptom mapping technique in a series of 54 patients with right-hemisphere stroke. Anatomical data indicated that lesions in the superior and middle temporal gyri, the basal ganglia, as well as the inferior occipitofrontal fasciculus are responsible for spatial neglect in both acute and chronic phases.We also had the opportunity to evaluate 69 patients with right brain lesions longitudinally. Our patients were admitted after a first right-hemisphere stroke (mean delay: 7.5 AE 14.6 days), at a mean age of 64.95 AE 14.6 years. Mean delay between the acute and chronic phase was 350.21 AE 184.7 days. These demographic data are comparable with the patients of Karnath et al. (2011). Neglect was considered as present when patients failed at least two out of eight tests (Table 1)-unlike diagnoses based on two out three tests in Karnath et al. (2011). In the acute phase, 31 patients had neglect (45%). In the chronic phase, 17 of these 31 neglect patients still showed a significant impairment (55%). Using the same voxel-wise lesion mapping as Karnath et al. (2011), we found partly different results, particularly in the acute phase (detailed below). However, we believe that major differences in the findings may depend on the clinical measures used to define neglect, since this syndrome may include heterogeneous symptoms.

Brain regions beyond visual cortex are thought to be responsible for attention-related modulation of visual processing [1, 2], but most evidence is indirect. Here, we applied functional magnetic resonance imaging (fMRI), including retinotopic mapping of visual areas, to patients with focal right-parietal lesions and left spatial neglect [3, 4]. When attentional load at fixation was minimal, retinotopic areas in right visual cortex showed preserved responses to task-irrelevant checkerboards in the contralateral left hemifield, analogously to left visual cortex for right-hemifield checkerboards, indicating a "symmetric" pattern in both hemispheres with respect to contralateral stimulation under these conditions. But when attentional load at fixation was increased, a functional asymmetry emerged for visual cortex, with contralateral responses in right visual areas being pathologically reduced (even eliminated for right V4/TEO), whereas left visual areas showed no such reduction in their contralateral response. These results reveal attention-dependent abnormalities in visual cortex after lesions in distant (parietal) regions. This may explain otherwise puzzling aspects of neglect [5, 6], as confirmed here by additional behavioral testing.

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this study is the first to report normative data on neuropsychological tests among children in Cameroon and constitutes an initial step for the advancement of neuropsychology in this country in particular and in sub-Saharan Africa in general. The battery is currently used in Cameroon with children suffering from Sickle Cell Disease as an aid to detect cerebrovascular complications.

Spatial neglect is a complex neuropsychological disorder, in which patients fail to detect and respond to contralesional stimuli. Recent studies suggest that these symptoms may reflect a combination of different component deficits, associated with different lesion substrates. Thus, damage to right lateral prefrontal and inferior parietal regions produce different degrees of left neglect on cancellation and line bisection tasks, respectively. Here we tested for dissociable behaviors across two tasks designed to assess distinct cognitive processes possibly mediating such components, in 14 patients with right focal lesion in either the frontal or parietal lobe. In the "distractor filtering" task, patients had to respond to a visual target presented centrally, with or without a lateralized distractor. Only frontal-lesioned patients showed a marked slowing of reaction times when a central target appeared with a simultaneous right distractor (compared to center and left distractor). In the "spatial coding" task, patients had to detect a target among successive visual stimuli presented horizontally with three sequence conditions (regular/predictive or irregular/non-predictive). Only parietal-lesioned patients were unable to benefit from the predictability of the target position, with similar reaction times across all sequence conditions. By contrast, frontal patients showed faster reaction times on trials with a regular succession of stimuli (compared to random order). Taken together, these results suggest that frontal damage may contribute to left inattention by disrupting top-down control and resistance to distractors on the ipsilesional side, whereas parietal damage may disrupt the maintenance of stable locations in space across gaze shifts or time. This further supports the notion that left neglect may arise as a combined breakdown or impaired connectivity between frontal and parietal mechanisms involved (respectively) in the selective control and memory storage components of spatial attention.

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