Abstract
Although aphasia and hemispatial neglect are classically labeled as cortical deficits, language deficits or hemispatial neglect following lesions to subcortical regions have been reported in many studies. However, whether or not aphasia and hemispatial neglect can be caused by subcortical lesions alone has been a matter of controversy. It has been previously shown that most cases of aphasia or hemispatial neglect due to acute non-thalamic subcortical infarcts can be accounted for by concurrent cortical hypoperfusion due to arterial stenosis or occlusion, reversible by restoring blood flow to the cortex. In this study, we evaluated whether aphasia or neglect occur after acute thalamic infarct without cortical hypoperfusion due to arterial stenosis or occlusion. Twenty patients with isolated acute thalamic infarcts (10 right and 10 left) underwent MRI scanning and detailed cognitive testing. Results revealed that 5/10 patients with left thalamic infarcts had aphasia and only 1 had cortical hypoperfusion, whereas 2/10 patients with right thalamic infarcts had hemispatial neglect and both had cortical hypoperfusion. These findings indicate that aphasia was observed in some cases of isolated left thalamic infarcts without cortical hypoerfusion due to arterial stenosis or occlusion (measured with time-to-peak delays), but neglect occurred after isolated right thalamic infarcts only when there was cortical hypoperfusion due to arterial stenosis or occlusion. Therefore, neglect after acute right thalamic infarct should trigger evaluation for cortical hypoperfusion that might improve with restoration of blood flow. Further investigation in a larger group of patients and with other imaging modalities is warranted to confirm these findings.
Highlights
The role of subcortical structures in cognitive processing remains somewhat elusive
Hypoperfusion was defined as >4 s mean delay in TTP arrival of contrast across voxels in the region of interest (ROI) relative to the homologous region in the non-ischemic hemisphere. This threshold was selected because it corresponds to dysfunctional tissue defined in our previous studies and defined by PET [52, 53]. For both left and right hemisphere stroke patients, we examined the entire cortex within the territory of the middle cerebral artery and posterior cerebral artery (PCA), as aphasia and neglect have been reported in association with lesions in each territory
The goal of the present study was to evaluate whether acute thalamic aphasia or neglect can be caused by cortical hypoperfusion due to large vessel stenosis or occlusion
Summary
The role of subcortical structures in cognitive processing remains somewhat elusive. Over the last decades, the advent of functional imaging has led to a better understanding of the role of subcortical structures in cognitive processing. The thalamus has been of particular interest to researchers given that it projects to all areas of the neocortex including those areas in the frontal, temporal, and parietal regions that are commonly associated with language and cognition. Many functional imaging studies of language reveal thalamic participation in a variety of tasks and processes [1,2,3,4,5,6,7,8,9,10]. A recent study reviewed the role of the thalamus in 50 functional imaging studies of language tasks [11]. The results of this literature review suggest that the thalamus may play a role in processes that involve the manipulation of lexical information, and that thalamic activation may be modulated by the difficulty of task demands. Language and cognitive deficits caused by stereotactic surgery (e.g., thalamotomy) or electric stimulation of the thalamus provided additional information about the role of specific thalamic nuclei in language and cognitive processes underlying language tasks [23,24,25,26]
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