Silent brain infarction (SBI) is an increasingly recognized, and yet still poorly understood, clinical disorder characterized by the often incidental finding of cerebral infarction on imaging in the absence of clinically apparent neurological deficit. Although first described ≈50 years ago by Fisher1 through autopsy studies, it was not until the development of more sensitive imaging modalities that their characterization has been possible.
Of the epidemiological literature available on SBI, the most credible and generalizable data come from representative community samples, from which the general population prevalence of SBI has been estimated as 10% to 20%, with longitudinal studies suggesting a yearly incidence of 3% to 4%.2 However, this climbs as high as 55% in clinical-based studies of otherwise healthy patients3 and is higher than 90% in certain disease-specific populations.4
Despite such a high prevalence, mounting evidence suggests that SBI is not a silent event at all but is associated with subtle neurological deficits, neurocognitive dysfunction, psychiatric disorders, an increased incidence of overt stroke, and early mortality. In light of these associations, it has been proposed that the designation silent be replaced with the term covert.5
The principle objective of this article is to review the current body of published medical research critically to (1) define SBI and highlight problems inherent in that definition; (2) examine the risk factors, incidence and prevalence of SBI; (3) assess theories on the underlying pathogenesis of SBI; and (4) discuss the clinical consequences of these lesions.