Cerebral blood flow by arterial spin labeling in poststroke dementia

Dementia is common in people with stroke and may be preexisting in 10% of subjects and a direct consequence of the stroke in a further 15%.1 However, stroke is also a risk factor for dementia in the long term.1,2 Alzheimer pathology may play an important role in the development of poststroke dementia (PSD), and risk factors for Alzheimer disease (AD) overlap with those for stroke.3,4 The incidence of AD increases strongly with age5 and may play a greater role in development of dementia in older stroke survivors. In AD, there is a well-established pattern of hypoperfusion or hypometabolism in the posterior cingulate, temporoparietal, and prefrontal cortices, with relative sparing of the primary sensory cortices.6 Reduced cerebral blood flow (CBF) has been reported in vascular dementia (VaD) compared with that in control subjects.7–9 Likewise, vascular cognitive decline has been associated with global hypoperfusion8,10 and specific reductions in the thalamus in studies of small vessel disease.7,9 The aim of this study was to measure CBF using arterial spin labeling MRI in older stroke survivors (aged older than 75 years) to compare CBF in those with vs those without subsequent dementia. We also compared them with subjects with AD and healthy control subjects. We hypothesized that the PSD group would have globally low perfusion, with thalamic deficits (possibly associated with subcortical stroke), whereas we expected the AD group to show hypoperfusion in the posterior parietal and prefrontal cortices. We expected medial temporal lobe atrophy to be marked in AD but also to be present in PSD because of the presence of Alzheimer-type pathology in this older group.