CONTINUING EDUCATION Cerebral microbleeds: a guide to detection and clinical relevance in different disease settings Andreas Charidimou & Anant Krishnan & David J. Werring & H. Rolf Jäger Received: 23 December 2012 / Accepted: 15 March 2013 # Springer-Verlag Berlin Heidelberg 2013 Abstract Cerebral microbleeds have emerged as an impor- tant new imaging marker of cerebral small vessel disease. With the development of MRI techniques that are exquisite- ly sensitive to paramagnetic blood products, such as T2*- weighted gradient-recalled echo and susceptibility-weighted sequences, microbleeds have been detected in ever- increasing numbers of patients in stroke and cognitive clinics, as well as in healthy older people and in a variety of other rarer diseases and syndromes. Detection of cerebral microbleeds has clinical implications with respect to the diagnosis of the underlying small vessel disease, the safety of antithrombotic use, and the risk of symptomatic intrace- rebral haemorrhage, cognitive impairment and dementia. This article provides a guide to the detection and clinical relevance of cerebral microbleeds in different conditions based on a comprehensive review of the literature and own findings in research and clinical practice. Keywords Cerebral microbleeds . Cerebral small vessel disease . Susceptibility-weighted imaging . Cerebral amyloid angiopathy . Intracerebral haemorrhage Background Since the first reports in the late 1990s [1, 2], publications on cerebral microbleeds (CMBs) have increased at an expo- nential rate, indicating that they are a focus of interest for neuroradiologists, neurologists and researchers in the field of cerebrovascular disease and dementia [3]. CMBs are defined as small, rounded, homogeneous, hypointense foci on T2*-weighed gradient-recalled echo (T2*-GRE) or susceptibility-weighted imaging (SWI) MRI sequences (Fig. 1 and Table 1)[4, 5]. Histopathological correlation studies suggest that radio- logically defined CMBs generally correlate well with small collections of blood-breakdown products, that have presum- ably leaked from damaged small vessels into the brain parenchyma [6, 7]. Fazekas et al. [6] first demonstrated in 11 autopsied brains that the pathological substrate of CMBs seen as hypointense lesions on T2*-GRE MRI, are focal accumulations of haemosiderin-laden macrophages. The subjects were mostly hypertensive patients who suffered an intracerebral haemorrhage (ICH): in the majority of the brains, CMBs were associated with hypertensive arteriopathy (in- cluding fibrohyalinosis), but in two brains, cerebral amyloid angiopathy (CAA) of variable extent was detected and found to be associated with blood leakage foci [6]. In the brains with underlying hypertensive vascular changes, CMBs were pref- erentially located in the basal ganglia and thalami, and less often in lobar (cortical or subcortical) areas [6]. A more recent study which combined SWI and histopathology in eight brains of Alzheimer ’ s disease patients [8] confirmed that CMBs correspond to areas of microscopic bleeding. A minority of these lesions were found to be microaneurysms, small lacunes Andreas Charidimou and Anant Krishnan contributed equally to this work. A. Charidimou : D. J. Werring Stroke Research Group, UCL Institute of Neurology, The National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK A. Krishnan : H. Rolf Jäger Lysholm Department of Neuroradiology, The National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK H. Rolf Jäger Department of Brain Repair and Rehabilitation, UCL Institute of Neurology, Queen Square, London WC1N 3BG, UK H. Rolf Jäger (*) UCL Institute of Neurology. The National Hospital for Neurology and Neurosurgery, University College Hospital (UCH), 8-11 Queen Square, Box 65, London WC1 N3BG, UK e-mail: r.jager@ucl.ac.uk Neuroradiology DOI 10.1007/s00234-013-1175-4