Abstract
Unilateral visual neglect is commonly defined as impaired ability to attend to stimuli presented on the side of visual space contralateral to the brain lesion. However, behavioral analyses indicate that different neglect symptoms can dissociate. The neuroanatomy of the syndrome has been hotly debated. Some groups have argued that the syndrome is linked to posterior parietal cortex lesions, while others report damage within regions including the superior temporal gyrus, insula, and basal ganglia. Several recent neuroimaging studies provide evidence that heterogeneity in the behavioral symptoms of neglect can be matched by variations in the brain lesions, and that some of the discrepancies across earlier findings might have resulted from the use of different neuropsychological tests and/or varied measures within the same task for diagnosing neglect. In this paper, we review the evidence for dissociations between both the symptoms and the neural substrates of unilateral visual neglect, drawing on ALE (anatomic likelihood estimation) meta-analyses of lesion-symptom mapping studies. Specifically, we examine dissociations between neglect symptoms associated with impaired control of attention across space (in an egocentric frame of reference) and within objects (in an allocentric frame of reference). Results of ALE meta-analyses indicated that, while egocentric symptoms are associated with damage within perisylvian network (pre- and postcentral, supramarginal, and superior temporal gyri) and damage within sub-cortical structures, more posterior lesions including the angular, middle temporal, and middle occipital gyri are associated with allocentric symptoms. Furthermore, there was high concurrence in deficits associated with white matter lesions within long association (superior longitudinal, inferior fronto-occipital, and inferior longitudinal fasciculi) and projection (corona radiata and thalamic radiation) pathways, supporting a disconnection account of the syndrome. Using this evidence we argue that different forms of neglect link to both distinct and common patterns of gray and white matter lesions. The findings are discussed in terms of functional accounts of neglect and theoretical models based on computational studies of both normal and impaired attention functions.
Highlights
The complexity of the visual world requires us to have the ability to select and process behaviorally relevant stimuli while ignoring the rest of the scene
We have previously demonstrated that, after right hemisphere damage, left allocentric neglect is associated with lesions to the right posterior superior temporal sulcus, angular, middle temporal/inferior temporal, and middle occipital gyri, while left egocentric neglect is linked to more right anterior lesions within perisylvian network including the middle frontal, postcentral, supramarginal, and superior temporal gyri as well as the insula (Chechlacz et al, 2010)
The inclusion criteria were as follows: (1) studies published in peer-reviewed journals; (2) use of lesion-symptom mapping approaches as defined in the Introduction, i.e., either lesion subtraction methods, VBM, or VLSM/VLBM methods; (3) the studied sample consisted of mainly brain injured patients and both experimental and control patients groups were described/defined clearly; (4) the findings were reported using spatial coordinates in either Montreal Neurological Institute (MNI; Evans et al, 1993) or Talairach space (Talairach and Tournoux, 1988); (5) papers defined neglect based on common assessment tools including at least one of the following: target cancelation, bisection, word reading, and figure copy
Summary
The complexity of the visual world requires us to have the ability to select and process behaviorally relevant stimuli while ignoring the rest of the scene. The unilateral neglect syndrome has a significant impact on daily activities and is correlated with poor recovery and return to independent living following the stroke (e.g., Campbell and Oxbury, 1976; Denes et al, 1982; Luaute et al, 2006). This disorder has a significant impact on the overall outcome following brain damage and has proved to be difficult to understand and treat (e.g., Kerkhoff, 2001; Parton et al, 2004; Singh-Curry and Husain, 2010)
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