Predictors and assessment of cognitive dysfunction resulting from ischaemic stroke

Abstract

Stroke remains a primary cause of morbidity throughout the world mainly because of its effect on cognition. Individuals can recover from physical disability resulting from stroke, but might be unable to return to their previous occupations or independent life because of cognitive impairments. Cognitive dysfunction ranges from focal deficits, resulting directly from an area of infarction or from hypoperfusion in adjacent tissue, to more global cognitive dysfunction. Global dysfunction is likely to be related to other underlying subclinical cerebrovascular disease, such as white-matter disease or subclinical infarcts. Study of cognitive dysfunction after stroke is complicated by varying definitions and lack of measurement of cognition before stroke. Additionally, stroke can affect white-matter connectivity, so newer imaging techniques, such as diffusion-tensor imaging and magnetisation transfer imaging, that can be used to assess this subclinical injury are important tools in the assessment of cognitive dysfunction after stroke. As research is increasingly focused on the role of preventable risk factors in the development of dementia, the role of stroke in the development of cognitive impairment and dementia could be another target for prevention.

Conflict of interest statement

Conflicts of interest

We have no conflicts of interest.

Copyright 2010 Elsevier Ltd. All rights reserved.

Figures

Figure 1. Cognitive deficits can be associated with areas of hypoperfusion that extend beyond the stroke lesion, as shown by the diffusion-perfusion mismatch on MRI

MRI sequences from an 85-year-old woman with stroke shows a relatively small right-sided subcortical infarct, but a large area of hypoperfusion. (A) DWI, with area of acute infarction. (B) Apparent diffusion coefficient map, obtained from DWI, showing the same region. (C) PWI time-to-peak map; the larger region (red) shows the area of hypoperfusion, and compared with DWI (A) shows a diffusion–perfusion mismatch, because the infarct size (on DWI) is much smaller than the area of abnormality on PWI. The right side of the brain is shown on the left side of the images, as per radiological convention. This patient had impaired performance on tests of hemispatial neglect, corresponding to the cortical hypoperfusion shown on PWI. DWI=diffusion-weighted imaging. PWI=perfusion-weighted imaging.

Figure 2. Cognitive deficits can be associated with white-matter tract damage, as shown with DTI

MRI scans, including apparent diffusion coefficient maps (top) and corresponding DTI scans (bottom), of a 56-year-old man who had a deep left internal capsule and corona radiata infarct 4 years previously. DTI shows degeneration of white-matter tracts, including the PTR, SS, and ILF. The degeneration of white-matter tracts might be responsible for the patient’s language deficits, including impairments in sentence repetition, comprehension of syntactically complex sentences, and production of grammatically complex sentences, which are generally attributable to cortical dysfunction. Alternatively, the language deficits might be due to left frontotemporoparietal cortical hypoperfusion on PWI (not shown), which in turn might have led to the degeneration of white-matter tracts. The right side of the brain is shown on the left side of the image, as per radiological convention. ACR=anterior corona radiata. ALIC=anterior limb of internal capsule. EC=external capsule. PLIC=posterior limb of internal capsule. PTR=posterior thalamic radiation. SS=sagittal striatum. ILF=inferior longitudinal fasciculus. SCR=superior corona radiata. PCR=posterior corona radiata. SLF=superior longitudinal fasciculus. DTI=diffusion tensor imaging.