Common and uncommon differential diagnosis of cerebral microhemorrhages

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1 Common and uncommon differential diagnosis of cerebral microhemorrhages Poster No.: C-0261 Congress: ECR 2014 Type: Educational Exhibit Authors: T. C. Rodrigues 1, S. B. Bergamaschi 1, C. F. R. B. Milito 2, C. S. Vergilio 1, R. S. de Carvalho 2, M. H. Idagawa 2 ; 1 São Paulo, SP/BR, 2 São Paulo/BR Keywords: DOI: Education, MR, CT, CNS, Neuroradiology brain, Hemorrhage /ecr2014/C-0261 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. Page 1 of 9

2 Learning objectives The most common causes of cerebral microhemorrhages (MHs) are systemic hypertension and amyloid angiopathy. Other less common causes include diffuse axonal injury, embolism, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), multiple cavernomas, vasculitis, metastasis and postradiation vasculopathy. Background Cerebral microhemorrhages are also known as microbleeds or lacunar hemorrhages. The cerebral microhemorrhages were defined as multiple foci of ovoid marked loss of signal intensity in weighted sequences in gradient-echo T2*. Should be differentiated from "flow void" vascular and cerebral calcifications, and also leptomeningeal hemosiderosis. Size criteria have been inconsistent. They are recognized as a marker of microangiopathy and have implications for diagnosis and prognosis. Imaging techniques: Computerized tomography (CT) without contrast and magnetic resonance imaging (MRI) of the brain. MRI is the most sensitive method for detection, particularly the gradient echo sequences - T2 * and ecoplanar - SWI (susceptibility-weighted imaging), where such injuries present with marked hypointense less than 10mm diameter. The SWI sequence still allows differentiation of calcification of bleeding. The greater sensitivity of MRI in the detection, arises from the "blooming effect" that makes the largest lesion in T2* sequence. Findings and procedure details 1. Amyloid Angiopathy (AA) Occurs by progressive deposition of amyloid within small and medium veins, leading to fibrinoid necrosis and vascular fragility. It's the major cause of lobar hemorrhage in the elderly, the number of MHs increase the risk of such bleeding. The presence of multiple strictly lobar hemorrhages (including MHs) demonstrated highly specific for AA in older patients without another set of intracranial hemorrhage causes (trauma, ischemic stroke, tumor, coagulopathy, or excessive anticoagulation). The distribution shows posterior Page 2 of 9

3 cortical predominance, tending to cluster in the same lobe in individuals with multiple lesions. 2. Hypertension Developed by intimal hyperplasia and hyalinosis in deep penetrating cerebral arterioles as a result of chronic hypertension. Unlike AA, in chronic hypertension are most commonly found in the thalamus, basal ganglia, cerebellum and pons. 3. Cavernous angioma It is a type of vascular malformation demonstrated on MRI as sinusoidal spaces and venous lakes, resembling "popcorn", which would globular areas of hyperintensity on T1 hypointense surrounded by halo on T2 *, representing hemosiderin deposited peripherally as a result of previous bleeding. 4. Diffuse axonal injury (DAI) Traumatic brain injury shear due to rapid acceleration or deceleration of the head most commonly in the gray/white junction, splenium of the corpus callosum and dorsolateral brainstem. It's seen as multiple small foci of hyperintensity on FLAIR, T2 and occasionally, the diffusion, due to the presence of white matter edema. It may be accompanied by MHs, and are more apparent in T2*weighted sequences and SWI. 5. CADASIL Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy is an inherited form of cerebral artery that leads to early demyelination and ischemic stroke. The underlying defect affects the smooth muscle cells of small vessels that are affected by type single negative amyloid angiopathy nonarteriosclerotic. MRI may show symmetric confluent areas of high signal intensity in the white matter in the frontal and anterior temporal lobe and within the external capsule. MHs have been reported in 25-70%, but have no characteristic distribution. 6. Embolism Hematogenous dissemination of septic emboli from bacterial, fungal and protozoal origin may even reach the cerebral vessels. 7. Metastasis It may manifest as MHs, more related tod melanoma and renal cell carcinoma. Page 3 of 9

interface the white / gray matter compatible with amyloid angiopathy Fig.

4 Images for this section: Fig. 1: MRI SWI sequence demonstrating multiple foci of marked hypointense distributed along the interface the white / gray matter compatible with amyloid angiopathy Fig. 5: MRI axial FLAIR sequences demonstrating extensive and confluent areas of hyperintense white matter and foci of microhemorrhages (arrows) in a patient with CADASIL. Page 4 of 9

2: Patient with hypertension history, with multiple foci of marked hypointense on SWI

5 Fig. 6: Patient with sepsis, with multiple foci spontaneously hyperdense on unenhanced CT, predominantly subcortical, suggestive of microhemorrhages by septic microemboli. Fig. 2: Patient with hypertension history, with multiple foci of marked hypointense on SWI predominating in the central brain region (arrows) compatible with micro-hemorrhages. Page 5 of 9

6 Fig. 3: MRI SWI sequence of a patient with multiple foci of low signal intensity scattered throughout the brain parenchyma in a case of cavernomatosis. Page 6 of 9

Fig. 4: Post-TBI patient with multiple foci with hypointense signal on T2* compatible with areas of micro-hemorrhages and possible mechanism of shear. Fig.

7 Fig. 4: Post-TBI patient with multiple foci with hypointense signal on T2* compatible with areas of micro-hemorrhages and possible mechanism of shear. Fig. 7: Axial MRI sequences showing marked hypointense foci (arrows) on gradient, with hyperintensity on T1 and enhancement after gadolinium contrast, compatible with microhemorrhages in metastatic melanoma. Page 7 of 9

8 Fig. 8: Cranial CT without contrast shows spontaneously hyperdense nodules (arrows) compatible with hemorrhagic metastases in patients with melanoma Page 8 of 9

9 Conclusion Radiological findings of brain cerebral microhemorrhages that may represent a specific underlying microscopic pathology: perivascular hemosiderin deposits. Careful study of its anatomical distribution helps clarify its histology meaning: the deeper may represent hypertensive vasculopathy and lobar, cerebral amyloid angiopathy. Furthermore presence of MHs can not only be a direct marker of small vessel disease prone to bleeding, but also an indicator of different types of microangiopathy and a predictor of additional hemorrhagic cerebral stroke. Personal information References 1.Marisa Kastoff Blitstein, Glenn A. Tung. MRI of Cerebral Microhemorrhages AJR:189, September Yoshito Tsushima, Jun Aoki, and Keigo Endo Brain Microhemorrhages Detected on T2*-Weighted Gradient-Echo MR Images.AJNR Am J Neuroradiol : Viswanathan A., Chabriat H. Cerebral microhemorrhage. Stroke Feb;37(2): Epub 2006 Jan 5. 4.Michele A. Scully, Gabrielle A. Yeaney, Margaret L. Compton, et al. SWAN MRI revealing multiple microhemorrhages secondary to septic emboli from mucormycosis. Neurology 2012;79; Barsottini OGP, Pereira JKD, Marques MCP, Idagawa MH, Ferraz HB. CASE REPORT. Palatal tremor: an unusual manifestation of CADASIL. Einstein. 2004; 2(4): Mittal S, Wu Z, Neelavalli J. Haacke EM. Susceptibility-weighted imaging: technical aspects and clinical applications, part 2. AJNR Am J Neuroradiol Feb;30(2): doi: /ajnr.A1461. Epub 2009 Jan 8. Page 9 of 9

CT and MR findings of systemic lupus erythematosus involving the brain: Differential diagnosis based on lesion distribution

CT and MR findings of systemic lupus erythematosus involving the brain: Differential diagnosis based on lesion distribution Poster No.: C-2723 Congress: ECR 2010 Type: Educational Exhibit Topic: Neuro