Atlas of Emergency Neurovascular Imaging by Yang Tang

Atlas of Emergency Neurovascular Imaging by Yang Tang

Author:Yang Tang
Language: eng
Format: epub
ISBN: 9783030436544
Publisher: Springer International Publishing


The sparing of deep gray matter and brain stem is the key differentiating feature from hypertensive hemorrhages. Besides CAA and hypertension, other common etiologies of intraparenchymal hemorrhage include vascular malformations (AVM, AVF, or cavernous malformation), underlying primary or metastatic tumors, coagulopathy, hemorrhagic transformation of ischemic infarction, cerebrovenous thrombosis, illicit drug use, etc. The differential diagnoses for multiple microhemorrhages include amyloid angiopathy, chronic hypertension, cavernous malformations, hemorrhagic metastasis, diffuse axonal injury, fat embolism, septic emboli, and vasculitis.

CAA is also a frequent cause of convexity subarachnoid hemorrhage and superficial siderosis in patients over 60 (Fig. 6.7b). Other etiologies for convexity SAH include trauma, cerebrovenous thrombosis, PRES, and RCVS.

CAA-related small vessel ischemic disease may cause progressive deep white matter FLAIR/T2 hyperintensity predominantly in the occipital lobes with sparing of subcortical U-fibers, as well as cortical microinfarcts [19].

CAA-related inflammation/angiitis occurs in many patients presenting with subacute cognitive impairment and seizure, due to immune response to the vascular deposits of amyloid. MRI shows a characteristic appearance of large, confluent, asymmetric T2 hyperintense lesions extending into the subcortical white and often the cortical gray matter in the pattern of vasogenic edema (Fig. 6.8). This can be confused with other entities such as encephalitis, neoplasm, or atypical PRES, though the presence of microhemorrhages within the area of edema is highly suggestive of CAA-related inflammation. This represents a treatable form of CAA as symptoms and edema are reversible after immunosuppressive therapy [20].

Fig. 6.8CAA-related inflammation. Patient presents with altered mental status and seizure. (a) FLAIR shows asymmetric vasogenic edema of the left cerebral hemisphere. (b) GRE sequence shows multiple lobar microbleeds from amyloid deposition



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