Emerging spectra of silent brain infarction.

S ilent 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 neurologi-cal deficit. Although first described ≈50 years ago by Fisher 1 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 patients 3 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 dysfunc-tion, 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. There is no universally accepted definition of SBI, which hampers attempts to characterize and investigate these lesions fully. In general, SBI has been described as cerebral infarcts that are observed on either computed tomographic or MRI scans in the absence of any corresponding, clinically apparent cerebrovascular ischemic event. The rigor with which corresponding clinical events are identified dramatically affects the reported incidence of SBI, and investigators have deviated widely in their means of clinical detection. In many studies, such events have been determined by self-report only or through retrospective medical record review. These methodologies are clearly subject to bias, given variability in the recall, presentation, and investigation of possible cerebrovascular events. Similarly, variations in diagnostic imaging strategies have important implications for estimates of SBI incidence and prevalence. MRI is now regarded as the imaging modality of choice for diagnosing SBI; however, significant interstudy differences exist in the application of this technology. Major sources …