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Neuroradiology Case of the Week
Case 368
December 2008
Daniel Ginat, MD, MS, Rajiv Mangla, MD
and Per-Lennart Westesson, MD, PhD, DDS
Clinical
Presentation:
Patient 1: An 88-year-old female with history of cerebral hemorrhage, presents with periods of confusion.
Patient 2: An 80-year-old male with a history of history of left frontal intracranial hemorrhage.
Imaging Findings:
CT findings in Patient 1: High attenuation focus in subcortical region of left parietal lobe, surrounded by mild edema suggests an acute hemorrhage attributable to amyloid angiopathy (Fig. 1).
MRI findings in Patient 2: Left frontal lobe clot, measuring 2 x 1.8 cm with high intensity on T1-weighted sequence related to methemoglobin formation. This hematoma is surrounded by hypodensity rim secondary to hemosiderin formation (Fig. 2). These changes are consistent with evolving left frontal hematoma.
Gradient echo images demonstrate multiple areas of signal drop in the left frontal, left parietal, bilateral occipital and temporal lobes most likely related to amyloid angiopathy (Fig. 3).
FLAIR (Fig. 4) and T2 weighted images demonstrate multiple hyperintensities in the periventricular white matter in centrum semiovale in the watershed region consistent with white matter small vessel disease and watershed old infarctions.
DWI also demonstrates increased signal intensity in the region of the evolving left frontal hematoma related to paramagnetic artifact (Fig. 5). Chronic lesions are not well visualized on this sequence.
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| Figure 1: Non-contrast head CT axial section demonstrates large subcortical acute hemorrhage in a lobar distribution. Generalized atrophy is also noted. |
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Figure 2: Axial T1WI demonstrates a subacute hemorrhage with a hypodense rim (arrow) in the region of the left frontal cortical-white matter junction.
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| Figure 3:
Coronal GRE image brings-out chronic lesions as hypointense foci. |
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Figure 4: Axial FLAIR demonstrates multiple high intensity lesions throughout the white matter bilaterally that represent old infarcts (red arrows) in addition to the large subacute hemorrhage in the left frontal lobe (blue arrow).
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| Figure 5: Axial DWI again demonstrates increased signal in the left frontal lobe. The old lesions seen on the FLAIR sequence at the corresponding level are not well visualized.
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Diagnosis: Cerebral amyloid angiopathy: acute, subacute, and chronic macrohemorrhages
Discussion: Cerebral amyloid angiography (CAA) is a disease of increased fragility that affects small to medium caliber vessels within the cortex and leptomeninges [1]. Decreased vessel elasticity attributed to deposition of beta-pleated amyloid protein within blood vessel media and adventitia results in microaneurysm production and fibrinoid degeneration. These pathologic changes predispose to hemorrhage, which typically occurs in a lobar distribution within the frontal and parietal lobes. Hemorrhage can occur as microhemorrhages (<5mm) and macrohemorrhages (>5mm) and can extend into the adjacent white matter. Occasionally, subarachnoid and subdural hemorrhage may result from extension of underlying bleed or when superficial vessels are involved. Multiple foci of hemorrhage may appear either synchronously or in different stages of activity. CAA increases in incidence with age, and is estimated to be the etiology of 38 to 74% cases of intracranial hemorrhage in the elderly [2]. Although frequently asymptomatic, symptoms may include headache, nausea and vomiting, loss of consciousness, focal neurological deficits, and seizures.
While CT is well-suited for detecting acute hemorrhages, old bleeds may not be readily apparent with this modality. However, MRI is better suited for delineating microhemorrhages and chronic hemorrhages, as well as the burden of ischemic sequelae [2]. On T2-weighted gradient-echo imaging hemosiderin produces characteristic signal dropout and is considered the most specific sequence for microhemorrhages in CAA. Nevertheless, CAA remains a diagnosis of exclusion. However, preliminary research using positron emission tomography with beta-amyloid binding compound shows promising results in enabling identification of beta amyloid in patients with cerebral amyloidosis angiopathy [3].
References:
- Grossman R. Yousem D. Neuroradiology, The Requisites. 2nd Ed. Mosby, Philadelphia, 2003: 606-607.
- Chao CP, Kotsenas AL, Broderick DF. Cerebral amyloid angiopathy: CT and MR imaging findings. Radiographics. 2006 Sep-Oct;26(5):1517-31. [PubMed]
- Johnson KA, Gregas M, Becker JA, et al. Imaging of amyloid burden and distribution in cerebral amyloid angiopathy. Ann Neurol. 2007 Sep;62(3):229-34. [PubMed]
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