Archief Roodbont

Abstract

In the last decade or so, cerebral microbleeds (CMBs) – tiny perivascular hemorrhages seen as small, well-demarcated, hypointense, rounded lesions on MRI sequences that are sensitive to magnetic susceptibility – have generated increasing interest among neurologists and clinical stroke researchers. As MRI techniques become more sophisticated, CMBs are increasingly detected in various patient populations (including all types of stroke, Alzheimer’s disease and vascular cognitive impairment) and healthy community-dwelling older people. Their presence raises many clinical dilemmas and intriguing pathophysiological questions. CMBs are emerging as an important new manifestation and diagnostic marker of cerebral small-vessel disease. They are a potential predictor of future intracerebral hemorrhage risk, a possible contributor to cognitive impairment and dementia and a potential key link between vascular and degenerative pathologies. In this article, we discuss the available pathological, neuroimaging and clinical studies in the field, and we provide a modern overview of the clinical and pathophysiological implications of CMBs in different disease settings.

Introduction

The past decade has witnessed increasing interest in cerebral microbleeds (CMBs), reflected by the proliferation of publications about them.^[1] CMBs are defined radiologically as small, rounded, homogeneous, hypointense lesions on T2*-weighed gradient-recalled echo (T2*-GRE) and related MRI sequences that are sensitive to magnetic susceptibility (Figure 1).^[2] Scharf et al. were the first to report on small, intracerebral black dots of signal loss on T2-weighted spin-echo MRI in patients with hypertensive cerebrovascular disease and intracerebral hemorrhage (ICH) associated with ischemic white matter disease and lacunar infarcts.^[3] They called these lesions ‘hemorrhagic lacunes’, and their further characterization using T2*-GRE MRI sequences led to the current radiologic definition of ‘microbleeds’, a term coined by Offenbacher and colleagues in 1996.^[4] A key feature of CMBs is that they are not seen well on conventional computed tomography or MRI scans (Figure 1). Available histopathological studies suggest that CMB radiological lesions are due to tiny bleeds adjacent to abnormal small vessels, being mainly affected by hypertensive angiopathy (arteriolosclerosis – usually lipohyaline degeneration related to hypertension) or cerebral amyloid angiopathy (CAA).^[5]