Arjen Lindenholz

135 Intracranial Atherosclerotic Burden and Cerebral Parenchymal Changes at 7T MRI 6 Introduction Intracranial atherosclerosis (ICAS) is an important cause of ischemic stroke. 1 Historically, ICAS has been evaluated by measuring the presence of intracranial stenosis using lumenographic techniques, or by detecting vessel wall calcifications that generally reflect a more advanced stage of ICAS. 2-5 Over the last two decades, however, intracranial vessel wall MRI sequences have enabled in vivo visualization of the intracranial vessel wall itself. 6-8 With these dedicated MRI sequences, both subtle (non-stenotic) and more advanced vessel wall pathology of the proximal cerebral large arteries can be assessed. Vessel wall changes of the large intracranial arteries are frequently observed on intracranial vessel wall MR images, both in patients with cerebrovascular disease as well as in healthy elderly individuals, but the nature and clinical relevance of these changes have not been fully established. 9-12 Ex vivo studies applying intracranial vessel wall MRI to postmortem samples suggest that these changes represent vessel wall disease at an early stage to halfway on the developmental timeline of ICAS. 13-18 At the end of this timeline, plaque disruption, thrombus formation and large vessel stenosis or occlusion can lead to transient ischemic attack (TIA) or ischemic stroke. The parenchymal consequences of vessel wall changes presumably reflecting less advanced ICAS, however, are less clear, hampering interpretation of these changes in clinical practice. ICAS in the smaller arteries, arterioles and capillaries – while difficult to visualize using vessel wall MRI due to their small caliber – or emboli disrupted from atherosclerotic plaques located in larger parent arteries may lead to (small) subcortical infarcts, deep grey matter infarcts, lacunes of presumed vascular origin, cortical microinfarcts or white matter hyperintensities. 19,20 Often, these cerebrovascular changes of the small vessels and their sequelae are categorized as a separate disease entity (small vessel disease, SVD) compared with large artery stroke, although both small and large cerebral arteries comprise one vascular bed that is physiologically connected, suggesting that pathology in one ‘type’ of vessel bed will inevitably affect the other. Recent studies have shown evidence for this connection: for example, large (intracranial) artery diseasemay result in endothelial damage and blood-brain barrier damage of the smaller arteries by the release of inflammatory molecules and enzymes, while alternatively, atherosclerotic plaques located in the larger intracranial arteries may obstruct orifices of smaller branching arteries resulting in small vessel pathology. 21,22 Nevertheless, the exact role and direction of effect – cerebrovascular changes of the small arteries by large artery pathology, vice versa, or bilateral – remains to be elucidated. 22