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Research ArticleBrain

MR Imaging Features of Amyloid-Related Imaging Abnormalities

J. Barakos, R. Sperling, S. Salloway, C. Jack, A. Gass, J.B. Fiebach, D. Tampieri, D. Melançon, Y. Miaux, G. Rippon, R. Black, Y. Lu, H.R. Brashear, H.M. Arrighi, K.A. Morris and M. Grundman
American Journal of Neuroradiology October 2013, 34 (10) 1958-1965; DOI: https://doi.org/10.3174/ajnr.A3500
J. Barakos
aFrom the California Pacific Medical Center (J.B.), San Francisco, California
bSynarc (J.B., Y.M.), Newark, California
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R. Sperling
cBrigham and Women's Hospital (R.S.), Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts
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S. Salloway
dWarren Alpert Medical School of Brown University (S.S.), Providence, Rhode Island
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C. Jack
eMayo Clinic (C.J.), Rochester, Minnesota
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A. Gass
fUniversity Hospital Mannheim (A.G.), University of Heidelberg, Mannheim, Germany
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J.B. Fiebach
gCenter for Stroke Research (J.B.F.), Charité, Berlin, Germany
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D. Tampieri
hNeuroRx Research (D.T., D.M.), Montreal, Quebec, Canada
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D. Melançon
hNeuroRx Research (D.T., D.M.), Montreal, Quebec, Canada
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Y. Miaux
bSynarc (J.B., Y.M.), Newark, California
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G. Rippon
iPfizer Inc (G.R., R.B.), Collegeville, Pennsylvania
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R. Black
iPfizer Inc (G.R., R.B.), Collegeville, Pennsylvania
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Y. Lu
aFrom the California Pacific Medical Center (J.B.), San Francisco, California
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H.R. Brashear
jJanssen Alzheimer Immunotherapy Research & Development, LLC (H.R.B., H.M.A., K.A.M., M.G.), South San Francisco, California
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H.M. Arrighi
jJanssen Alzheimer Immunotherapy Research & Development, LLC (H.R.B., H.M.A., K.A.M., M.G.), South San Francisco, California
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K.A. Morris
jJanssen Alzheimer Immunotherapy Research & Development, LLC (H.R.B., H.M.A., K.A.M., M.G.), South San Francisco, California
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M. Grundman
jJanssen Alzheimer Immunotherapy Research & Development, LLC (H.R.B., H.M.A., K.A.M., M.G.), South San Francisco, California
kGlobal Partners Inc (M.G.), Cambridge, Massachusetts.
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    Fig 1.

    ARIA-E (effusion); sulcal FLAIR hyperintensity. FLAIR MR imaging at baseline (A) and week 19 (B). On the follow-up surveillance scan (week 19), sulcal FLAIR hyperintensity developed in the right frontal region (arrow). No associated signal abnormality was identified on other imaging sequences, including T1 and gradient recalled-echo/T2* imaging (not shown). Because the imaging appearance mimicked that of a subarachnoid hemorrhage, CT and lumbar puncture were performed, both of which had normal findings, revealing no evidence of blood products.

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    Fig 2.

    ARIA-E (edema and effusion); parenchymal and sulcal FLAIR hyperintensity. FLAIR sequences at baseline (A), week 19 (B), and week 32 (C). By week 19 (6 weeks after the second dose of bapineuzumab), a zone of cortical swelling, sulcal effacement, and parenchymal hyperintensity has developed in the right temporal-occipital lobe. A small sulcal effusion and faint overlying linear leptomeningeal hyperintensity (arrows) help define the area of abnormality. By week 32, these findings have largely resolved. As is typically the case with bapineuzumab-related ARIA, the patient remained asymptomatic throughout all imaging time points.

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    Fig 3.

    ARIA-E (edema); week 19 parenchymal FLAIR hyperintensity. Week 19 FLAIR (A) and corresponding DWI (B) and week 19 gadolinium (C). On the surveillance scan for week 19 (A), several large regions of parenchymal edema develop, principally in the bifrontal and left temporal regions, which resolve on follow-up (not shown). Week 19 DWI reveals minimal T2 shinethrough (B), but no ADC abnormality (not shown). With gadolinium, there is no frank enhancement with only mild prominence of overlying cortical vasculature, in keeping with nonspecific cerebral swelling (C).

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    Fig 4.

    ARIA-E (edema) with incident ARIA-H (microhemorrhages). FLAIR and corresponding gradient recalled-echo/T2* sequences of the same patient, at baseline (A and B) and week 19 (C and D). By week 19 (6 weeks after the second dose of bapineuzumab), significant right-hemispheric edema has developed. As is characteristic of ARIA-E, despite the extensive parenchymal changes, DWI and ADC findings remained normal (not shown), confirming these findings as reflecting vasogenic as opposed to cytotoxic edema. On the corresponding gradient recalled-echo/T2* images, there is concomitant development of several punctate microhemorrhages in the right parietal region (circle). On subsequent imaging, the cerebral edema resolved while the microhemorrhages remained stable (not shown). In general, the severity of ARIA changes was associated with both Apolipoprotein ε4 allele status and drug dosage. As such, this patient was an Apolipoprotein ε4 homozygote and in the highest drug-dose arm.

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    Fig 5.

    ARIA-E (edema) with incident ARIA-H (superficial hemosiderin deposits). Gradient recalled-echo/T2* and corresponding FLAIR sequences from the same patient, at baseline (A), week 19 (B), and week 28 (C). By week 19 (B), several regions of parenchymal edema have developed, including bifrontal regions and the right parieto-occipital lobe. On the corresponding gradient recalled-echo/T2* images, by week 19, there is concomitant development of several superficial linear areas of blood-degradation products (arrows) in the bifrontal regions (≥10 mm). By week 28, the FLAIR changes relating to ARIA-E have resolved, with blood products re-demonstrated.

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    Table 1:

    Clinical characteristics of ARIA

    ARIA ComponentPrimary Diagnostic Imaging SequenceNature of Leakage ProductsLocation of Increased Vascular Permeability
    ParenchymaLeptomeninges
    ARIA-EFLAIRProteinaceous fluidVasogenic edemaSulcal effusion/exudate
    ARIA-HGRE/T2*Heme productsMicrohemorrhage (hemosiderin deposits <10 mm or large hemosiderin deposits ≥10 mm)Superficial hemosiderin deposits
    • Note:—GRE indicates gradient recalled-echo.

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    Table 2:

    Results

    ARIA Type: IncidenceLocation: Isolated LeptomeningealLocation: Isolated ParenchymalLocation: Combined
    ARIA-E: 36/210 (17%)ARIA-E: sulcal effusion: 15/36 (42%)ARIA-E: parenchymal edema: 8/36 (22%)ARIA-E: effusion and edema combined: 13/36 (36%)
    ARIA-H: 26/210 (12.4%)ARIA-H: superficial hemosiderin deposit: 2/26 (8%)ARIA-H: parenchymal microhemorrhage: 24/26 (92%)
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American Journal of Neuroradiology: 34 (10)
American Journal of Neuroradiology
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1 Oct 2013
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Cite this article
J. Barakos, R. Sperling, S. Salloway, C. Jack, A. Gass, J.B. Fiebach, D. Tampieri, D. Melançon, Y. Miaux, G. Rippon, R. Black, Y. Lu, H.R. Brashear, H.M. Arrighi, K.A. Morris, M. Grundman
MR Imaging Features of Amyloid-Related Imaging Abnormalities
American Journal of Neuroradiology Oct 2013, 34 (10) 1958-1965; DOI: 10.3174/ajnr.A3500

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MR Imaging Features of Amyloid-Related Imaging Abnormalities
J. Barakos, R. Sperling, S. Salloway, C. Jack, A. Gass, J.B. Fiebach, D. Tampieri, D. Melançon, Y. Miaux, G. Rippon, R. Black, Y. Lu, H.R. Brashear, H.M. Arrighi, K.A. Morris, M. Grundman
American Journal of Neuroradiology Oct 2013, 34 (10) 1958-1965; DOI: 10.3174/ajnr.A3500
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