Microhaemorrhages Or Microhaemorrhages?

Abstract Background As more patients have magnetic resonance imaging (MRI) brain undertaken, the identification of cerebral microhaemorrhages (CMHs) has increased. The modified Boston Criteria 2.0 standardises the diagnosis of cerebral amyloid angiopathy (CAA) as microhaemorrhage aetiology, and have moderately specific (83.5%) with low sensitivity (38.8%). CAA neuropathology is characterised by progressive deposition of beta-amyloid (Aβ) into cortical and leptomeningeal arteriolar walls. Neurochemical dementia diagnostic biomarkers bare the potential for assisting diagnosis. A CSF Aβ40 decrease more than Aβ42, and tau elevation, is characteristic of CAA. This case series highlights the diagnostic quandaries that arise in clinical practice. Case 1: 76year old female with multiple CMHs supratentorially and infratentorially. Metallic mitral valve replacement in situ. MRI susceptibility weighting imaging suggestive of CAA, with disproportionate cerebellar hemisphere and cortical involvement. No superficial siderosis. Case 2: 78year old male with previous thoracic aortic aneurysmal repair. Possible CAA was suggested on MRI with multiple foci of CMHs, dominantly peripherally and cortically, multiple areas of cerebral cortical infarction and bilateral cerebellar ischaemia. No superficial siderosis. MRI brain 7years prior, at the time of vascular surgery, had one lacunar acute infarct only. Case 3: 79year old male with multiple peripheral and dominantly posterior CMHs using Tacrolimus immunosuppression for renal transplant with possible CAA considered on 3Tesla MRI brain report. No superficial siderosis. Prescribed Apixaban for atrial fibrillation. Cerebrovascular small vessel disease was present and a right thalamic lacunar infarct. Methods Geriatrician and neuroradiologist case reviews. Results Case 1: CMH pattern post-metallic valve insertion can mimic CAA. Case 2: CMH pattern in thoracic aortic surgery can mimic CAA. Case 3: CMH pattern in Tacrolimus induced neurotoxicity can mimic CAA. Conclusion MRI has a role in discriminating between aetiologies of CMHs. The likelihood of CAA has clinical management implications. Access to CSF Aβ and tau sampling could assist diagnosis.