Chapter 27 Lacunes and lacunar syndromes

Abstract

Publisher Summary This chapter overviews the lacunar infarction (LF) and its clinical expression, lacunar syndromes, and reviews some historical aspects of such issues as response to therapy. There are two competing theories for the development of lacunes, infarction versus destructive invagination. In studies using risk-factor-free ischemic subtype definitions there was only a marginal excess of hypertension in lacunar versus non-lacunar infarcts. Diabetes is a well-known cause of small-vessel disease and would therefore be more likely to be a risk factor for LF. Smoking is also an established risk factor for LF. A number of studies on the genetics of LF have identified a series of markers, including mitochondrial DNA 16189 T to C variant, polymorphism of the interleukin-6 gene, endothelial nitric oxide haplotypes, and tissue plasminogen activator (tPA) polymorphism, which seem to be associated distinctly with lacunar syndromes, more so than other ischemic stroke syndromes. Given the importance of blood pressure inferred from the early findings of Fisher, and that lipohyalinosis was an important part of the lacunar infarction story. The application of modern imaging techniques to the LF issue is discussed. It was shown that some lacunar syndromes were associated with multiple lacunar infarcts on MR Diffusion Weighted Imaging, thus suggesting that emboli could be responsible for a proportion of patients presenting with lacunar syndromes. The clinical expression of lacunar infarcts relates to the site of infarction and, to some extent, the mechanism of infarction. The chapter discusses the classic lacunar syndromes such as pure motor hemiparesis, ataxic hemiparesis, dysarthria–clumsy hand syndrome, pure sensory stroke, sensorimotor stroke, and a variety of other lacunar syndromes.