Silent Cerebral Infarction

See related article, pages 2929–2935. The clinical event of stroke is not always a good guide to the existence of cerebral infarction. The advent of widespread neuroimaging has made this clear: up to one-third of patients with TIA and no physical examination changes have infarcts on scans.1 These patients are at even higher risk for subsequent stroke1 as are other patients with silent cerebral infarction.2 In consequence, silent cerebral ischemia is recognized as part of a spectrum of cerebrovascular disease, which also includes TIA to stroke. In this issue of Stroke , Das et al3 contribute to our understanding of silent cerebral infarction by evaluating its prevalence and correlates infarcts in the Framingham Offspring study. They report a prevalence of 10.7% among >2000 mid-life (mean age, 61 years), community-dwelling people who were clinically stroke-free. Das et al3 propose that only some vascular risk factors are linked to silent cerebral infarction.The strengths of the Framingham data are well-known, and this report from the Offspring study joins what are literally generations of others from that impressive investigation in building a better understanding of the interplay between vascular risk factors and adverse events. Inevitably, the results raise additional questions. Some, such as understanding the impact of silent cerebral infarction on outcomes in this sample—ie, what difference did these silent infarcts make to those who had them?—accept the premises of the study. But there is merit, too, in pursuing other questions that arise from these data, even when these questions reflect uncertainty about the starting assumptions that first motivated the inquiry reported here.To begin, what makes cerebral infarction silent? The Framingham data collection protocol used a time-based definition of stroke as “rapidly developing signs of focal neurological disturbance of presumed vascular etiology lasting more than 24 …