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Original Report |
1 Department of Radiology, Mayo Clinic, 4500 San Pablo Rd., Jacksonville, FL
32224-1865.
2 Department of Neurology, Mayo Clinic, Jacksonville, FL 32224-1865.
Received August 5, 2003;
accepted after revision November 25, 2003.
Address correspondence to D. F. Broderick.
Abstract
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CONCLUSION. The addition of gradient-refocused echo sequences to routine brain MRI resulted in the identification of cerebral amyloid angiopathy–related microbleeding in 15.5% of elderly patients. In most (86.7%) of these patients with positive findings, cerebral amyloid angiopathy was not suspected clinically, and 46.7% of these patients were undergoing anticoagulant or aspirin therapy, placing them at an increased risk of recurrent intracranial hemorrhage and catastrophic stroke.
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Small amounts of cerebral microbleeding are difficult to detect with T1- and T2-weighted sequences and are best shown on gradient-refocused echo MRI [4, 5]. After intracerebral hemorrhage, hemosiderin is deposited around the hemorrhage, causing a small drop in signal intensity on conventional T2-weighted images, but marked signal hypointensity on T2*-weighted gradient-refocused echo images. This prominent signal loss on the gradient-refocused echo images is caused by increased sensitivity to magnetic susceptibility induced by static field inhomogeneities arising from paramagnetic blood breakdown products. Although T2-weighted fast spin-echo sequences are much more commonly used than T2-weighted conventional spin-echo sequences because of faster acquisition times, the sensitivity of the fast spin-echo images to blood products is less than that of conventional spin-echo images. Gradient-refocused echo has been shown to be more sensitive than conventional spin echo and significantly more sensitive than fast spin-echo sequences [4]. Gradient-refocused echo is also more sensitive and shows better resolution in detecting hemorrhagic lesions than B0 diffusion-weighted echoplanar sequences [5].
Development of cerebral amyloid angiopathy is not correlated with the presence of common cerebrovascular risk factors including hypertension, diabetes mellitus, and hyperlipidemia [1, 2]. Although hypertension is far more frequently associated with small intracranial hemorrhages than cerebral amyloid angiopathy is, these hemorrhages typically occur in a pattern distinct from cerebral amyloid angiopathy–related intracerebral hemorrhages, predominantly in the basal ganglia, thalamus, brainstem, and cerebellum [1, 2]. Cerebral microhemorrhages resulting from diffuse axonal injury also occur in a different location, typically at the junction of gray and white matter [6].
Cerebral amyloid angiopathy is associated with increasing age, and autopsy studies have shown an incidence of cerebral amyloid angiopathy in 4.7–9% of patients 60–69 years old, and in 43–58% of patients more than 90 years old [2]. In a study of autopsied brains, Vonsattel et al. [3] found that cerebral hemorrhages resulting from cerebral amyloid angiopathy are peripherally located in the cortex, subcortex, and leptomeninges. Unfortunately, no imaging techniques are currently available for the direct visualization of amyloid, and the incidence of cerebral amyloid angiopathy–related cortical cerebral microbleeding is difficult to specify because definite diagnosis can only be made using biopsy or autopsy results [7]. However, using gradient-refocused echo imaging, cortical cerebral microbleeding occurring in a lobar distribution suggestive of cerebral amyloid angiopathy has been reported in 6.4% of 280 healthy patients 44–79 years old [8]. Recurrence of cerebral amyloid angiopathy–related cerebral microbleeding is common (19–21% 2-year recurrence rate) and is associated with increased morbidity and mortality [2]. Patients taking anticoagulants or aspirin are especially at risk for recurrent, potentially devastating intracranial hemorrhages [9, 10]. Currently, no treatment is available to halt or reverse the deposition of ß-amyloid protein.
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We defined cortical cerebral microbleeding as round 2- to 5-mm foci of decreased signal on gradient-refocused echo sequences occurring in a lobar–cortical distribution. Reviewers were unaware of patient history, prior MRI reports, and the interpretation of the other reviewer. A positive rating for cerebral amyloid angiopathy was assigned to examinations in which single or multiple cortical cerebral microbleeding was found (Fig. 1A, 1B, 1C). A negative rating was assigned to those examinations in which no cortical cerebral microbleeding was observed. Cases in which the reviewers disagreed were resolved by consensus. Patient records were reviewed to determine whether cerebral amyloid angiopathy was suspected clinically or previously proven by biopsy. Anticoagulation or aspirin therapy at the time of the MRI examination was also determined. Fisher's exact test was used to compare the use of anticoagulants and aspirin in each group.
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Cerebral microbleeding is suggestive of cerebral amyloid angiopathy when it occurs in a lobar–cortical distribution [3] and has been best shown with the gradient-refocused echo sequence [4, 5]. Cerebral amyloid angiopathy is prevalent in elderly patients and is associated with Alzheimer's disease [1, 2], but the number of cases of cerebral amyloid angiopathy discovered through routine screening using gradient-refocused echo sequences has not been extensively evaluated. In the Austrian Stroke Prevention Study, Roob et al. [8] evaluated 280 healthy patients (44–79 years old) using gradient-refocused echo MRI and found cerebral microbleeding in 18 patients (6.4%). Our screening of an elderly population showed a 15.5% incidence of cortical–lobar cerebral microbleeding. This percentage is higher than the incidence of 6.4% reported in the study by Roob et al., but they evaluated a younger population (44–79 years old) of healthy patients.
Interestingly, only two (13.3%) of our patients with positive findings had mention of possible cerebral amyloid angiopathy in their medical records, even though four (26.7%) did have symptoms of dementia. Consequently, the referring clinician did not consider a diagnosis of cerebral amyloid angiopathy in a majority (86.7%) of the positive patients at the time of the brain MRI.
Of the 15 patients with positive findings, four (26.7%) were undergoing anticoagulation therapy at the time of their brain MRI and three others (20%) were taking aspirin. Of the 82 patients with negative findings, seven (8.5%) were undergoing anticoagulation therapy and 34 (41.5%) were taking aspirin (Fig. 4). No statistical difference was apparent between the two groups in the use of warfarin sodium or aspirin. Greenberg et al. [11] have reported recurrent intracranial hemorrhage in 38% (9/24) of cerebral amyloid angiopathy patients on follow-up gradient-refocused echo MRI performed within 1.5 years after the first hemorrhage. Cerebral amyloid angiopathy patients are at an even greater risk for recurrent intracranial hemorrhage when taking anticoagulants or aspirin [9, 10]. Thus, the high incidence of cerebral microbleeding and associated anticoagulant or aspirin therapy in our study raises the question of the potential benefit of identifying patients with clinically unsuspected cerebral amyloid angiopathy. Even though no treatment is currently available and anticoagulants often cannot be discontinued because of other serious medical conditions, the risk of initiation or continuation of anticoagulants or aspirin should be carefully considered in those patients positive for cerebral microbleeding. McCarron et al. [10] recommend caution with anticoagulant and antiplatelet use in elderly patients with transient neurologic deficits and no significant carotid stenosis. We currently report findings positive for cortical cerebral microbleeding suggestive of cerebral amyloid angiopathy to the referring physician so that they may more completely assess the risks of continuing or initiating anticoagulant or aspirin therapy.
Two weaknesses of our study are a relatively small sample size and limited follow-up of those patients who were positive for cortical cerebral microbleeding. Our practice has a sizable elderly population, and although our sample size was somewhat limited, the high percentage of elderly patients is representative of our patient population. Our clinic also receives a heavy volume of referral patients from distant sites who are evaluated at our clinic but return home for their continuing care. Consequently, we did not include follow-up imaging as part of our study.
Despite these limitations, we conclude that with minimal extra time, the addition of routine gradient-refocused echo sequences to routine brain MRI is effective in identifying a silent and sizable subpopulation of elderly patients with cerebral microbleeding in a cortical distribution that is suggestive of cerebral amyloid angiopathy. Additionally, a significant proportion of the elderly patients in our study who showed cortical cerebral microbleeding were receiving anticoagulants or aspirin therapy, which places them at increased risk for recurrent, potentially devastating, intracranial hemorrhages. Further studies with larger patient populations and clinical and MRI follow-up are required to substantiate that these findings have value in clinical decision making.
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