Subcortical aphasia and neglect in acute stroke: the role of cortical hypoperfusion

Abstract

We have hypothesized that most cases of aphasia or hemispatial neglect due to acute, subcortical infarct can be accounted for by concurrent cortical hypoperfusion. To test this hypothesis, we demonstrate: (i) that pure subcortical infarctions are associated with cortical hypoperfusion in subjects with aphasia/neglect; (ii) that reversal of cortical hypoperfusion is associated with resolution of the aphasia; and (iii) that aphasia/neglect strongly predicts cortical ischaemia and/or hypoperfusion. We prospectively evaluated a consecutive series of 115 patients who presented within 24 h of onset or progression of stroke symptoms, with MRI sequences including diffusion weighted imaging (DWI) and perfusion weighted imaging (PWI), and detailed testing for aphasia or hemispatial neglect. The association between aphasia or neglect and cortical infarct (or dense ischaemia) on DWI and cortical hypoperfusion indicated by PWI, was evaluated with chi-squared analyses. Fisher exact tests were used for analyses with small samples. Cases of DWI lesion restricted to subcortical white matter and/or grey matter structures (n = 44) were examined for the presence of aphasia or neglect, and for the presence of cortical hypoperfusion. In addition, subjects who received intervention to restore perfusion were evaluated with DWI, PWI, and cognitive tests before and after intervention. Finally, the positive predictive value of the cognitive deficits for identifying cortical abnormalities on DWI and PWI were calculated from all patients. Of the subjects with only subcortical lesions on DWI in this study (n = 44), all those who had aphasia or neglect showed concurrent cortical hypoperfusion. Among the patients who received intervention that successfully restored cortical perfusion, 100% (six out of six) showed immediate resolution of aphasia. In the 115 patients, aphasia and neglect were much more strongly associated with cortical hypoperfusion (chi(2) = 57.3 for aphasia; chi(2) = 28.7 for neglect; d.f. = 1; P < 0.000001 for each), than with cortical infarct/ischaemia on DWI (chi(2) = 8.5 for aphasia; chi(2) = 9.7 for neglect; d.f. = 1; P < 0.005 for each). Aphasia showed a much higher positive predictive value for cortical abnormality on PWI (95%) than on DWI (62%), as did neglect (100% positive predictive value for PWI versus 74% for DWI). From these data we conclude that aphasia and neglect due to acute subcortical stroke can be largely explained by cortical hypoperfusion.

Anatomical Correlates of Directional Hypokinesia in Patients with Hemispatial Neglect

“…Damage to one node of the network produces widespread functional impairment in other nodes of the network, which may in turn result in similar behavioral deficits. In support of this view, blood flow studies indicate that subcortical lesions cause cortical hypoperfusion (Perani et al, 1987;Vallar et al, 1988;Hillis et al, 2002Hillis et al, , 2005. In particular, basal ganglia lesions that cause neglect are associated with abnormal perfusion of the superior temporal gyrus, inferior parietal lobule, and inferior frontal gyrus (Karnath et al, 2005).…”

Anatomy of Spatial Attention: Insights from Perfusion Imaging and Hemispatial Neglect in Acute Stroke

“…In the gap-detection test, there were three percentage-of-error scores: percentage of circles omitted (no response to the stimulus), percentage of left gaps missed, and percentage of right gaps missed, among the stimuli for which there was some response (an error consisted of incorrectly circling a circle with a gap). No normal subject made Ͼ10% errors on any of these tests (Hillis et al, 2000(Hillis et al, , 2002; therefore, neglect was defined as Ͼ10% errors on the task, with a simple majority of errors on the left. For line bisection, neglect was defined as deviation to the right by Ͼ10% of line length.…”

Global aphasia without hemiparesis: lesion analysis and its mechanism in 11 Korean patients

“…This is particularly crucial for acute aphasia, when a defect detected by CT and MRI cannot be reliably used to differentiate various aphasia types [4]. Moreover, SPECT can be used to identify the remote effects of vascular lesions [5]. Therefore, DWI and SPECT together may provide instructive clues for understanding the lesion profile of GAWH and the functional anatomy of aphasia.…”