Differential white matter involvement associated with distinct visuospatial deficits after right hemisphere stroke

Abstract

Visuospatial attention depends on the integration of multiple processes, and people with right hemisphere lesions after a stroke may exhibit severe or no visuospatial deficits. The anatomy of core components of visuospatial attention is an area of intense interest. Here we examine the relationship between the disruption of core components of attention and lesion distribution in a heterogeneous group (N = 70) of patients with right hemisphere strokes regardless of the presence of clinical neglect. Deficits of lateralized spatial orienting, measured as the difference in reaction times for responding to visual targets in the contralesional or ipsilesional visual field, and deficits in re-orienting attention, as measured by the difference in reaction times for invalidly versus validly cued targets, were measured using a computerized spatial orienting task. Both measures were related through logistic regression and a novel ridge regression method to anatomical damage measured with magnetic resonance imaging. While many regions were common to both deficit maps, a deficit in lateralized spatial orienting was more associated with lesions in the white matter underlying the posterior parietal cortex, and middle and inferior frontal gyri. A deficit in re-orienting of attention toward unattended locations was associated with lesions in the white matter of the posterior parietal cortex, insular cortex and less so with white matter involvement of the anterior frontal lobe. An hodological analysis also supports this partial dissociation between the white matter tracts that are damaged in lateralized spatial biases versus impaired re-orienting. Our results underscore that the integrity of fronto-parietal white matter tracts is crucial for visuospatial attention and that different attention components are mediated by partially distinct neuronal substrates.

Keywords: Hemispatial neglect; Logistic regression; Stroke; Visuospatial attention; White matter.

Figure 1

Stroke lesion distribution. A conjunction map of the right hemisphere stroke lesions in 70 subjects. Color scale indicates number of subjects with lesion at that voxel.

Figure 2

Effect of right hemisphere lesions on core components of attention. A. Timeline of stimulus presentation in the computerized spatial reorienting task. B. Field Effect and Validity Effect in msec in healthy age-matched controls and in stroke; AMC: age-matched controls; * = p < 0.01; ** = p < 0.001.

Figure 3

Relationship between Field Effect and Validity Effect.

Figure 4

Whole-brain voxel-wise logistic regression maps relating lesion location to behavior. Both Field Effect and Validity Effect were entered into the model and regressed against the stroke lesion distribution. The results are z statistic maps for each behavior showing the likelihood that a given voxel will be damaged if that behavior is impaired. A. Field Effect; B. Validity Effect; C. Conjunction (Green = Field Effect; Blue = Validity Effect; Red = Overlap) Maps are Monte Carlo-corrected for multiple comparisons (p<0.05) with z threshold=3. Ant Ins: anterior insula; IFG: inferior frontal gyrys; MFG: middle frontal gyrus; pIPS: posterior intraparietal sulcus; preCe: pre-central sulcus; TPJ: temporo-parietal junction.

Figure 5

Ridge regression maps relating lesion location to behavior: The color scale indicates weights (u) determined by ridge regression for the Field Effect and the Validity Effect. A. Field Effect; B. Validity Effect; C. Conjunction (Red = Field Effect; Blue = Validity Effect; Gray = Overlap).

Figure 6

Tract-wise lesion-deficit correlations. For each tract, the correlation between damage to that tract and the Field Effect and the Validity Effect are shown. After correcting for lesion size, time since stroke and multiple comparisons, correlations are not statistically significant taken individually. Tracts are ordered by strength of the correlation with the Field Effect. Results suggest damage to some tracts may be more highly correlated with one deficit or the other. Only tracts which sustained damage in this sample are shown.