**5. Management prospect and prognosis**

Chronic subarachnoid hemorrhage (cSAH) and superficial siderosis are quite characteristic of CAA. cSAH often results from lobar ICH extending to the cortical surface (Figure 4). Cortical superficial siderosis describes hemosiderin deposition in the superficial layers of the cerebral cortex and may follow repeated episodes of bleeding in the subarachnoid space. On T2\* weighted GRE sequence, cortical superficial siderosis shows a characteristic gyriform pattern

**Figure 4.** T2\*-weighted gradient-echo MR image of same patient as in figure 1, shows two linear areas of signal void (thin arrows) in the vicinity of large primary lobar hemorrhage (thick arrow) suggest chronic subarachnoid hemor‐

MRI is also sensitive for identifying CAA-related inflammation and ischemic changes and assessment of disease progression. [19] Leukoaraiosis, a radiological term which describes imaging changes in deep cerebral white matter, is a nonspecific finding seen in patients with CAA and can be due to demyelination, infarction or edema. On imaging, leukoaraiosis appears as patchy or confluent, CT hypodense or T2/FLAIR (fluid attenuated inversion recovery) hyperintense white matter abnormality with or without sparing of subcortical U fibers (Figure 5). Leukoaraiosis with sparing of U fibers is secondary to ischemic white matter damage and is seen in association with long standing dementia; whereas, white matter changes that extend to involve the U fibers are common in patients with subacute cognitive decline and are associated with mass effect due to inflammatory edema. [20,21] White matter changes in CAA increases over time and is an important contributor to overall disease burden. The CAA should be considered in the broad differential diagnosis of leukoencephalopathy especially if

associated with progressive dementia or cognitive impairment. [13]

of hypointense signal. [18]

46 Intracerebral Hemorrhage

rhage and cortical superficial hemosiderosis.

Currently, there is no treatment to halt or reverse β-amyloid deposition. Thus, attention is directed instead to the prevention of adverse outcomes associated with CAA, such as recurrent hemorrhages or progressive dementia. In this context, MRI may help in selecting patients for different types of secondary prevention of stroke. MR evidence of higher number of chronic microbleeds on baseline GRE MR images are predictive of a greater risk of recurrent hemor‐ rhage and future cognitive impairment. A routine use of GRE MRI sequence is suggested to detect microbleeds in older people to avoid potentially dangerous anticoagulant or antiplatelet therapy. [22]

The role of neurosurgery in ICH remains to be defined clearly. However, hematoma evacuation appears relatively safe in patients <75 years of age without intraventricular extension. [23] For future treatment of CAA, it is important to identify patients early in the course of disease before ICH or dementia occurs, to allow the use of disease modifying therapies. [24] Tramiprosate has been found to be a safe treatment option for patients with suspected CAA. Tramiprosate is an ionic compound that binds with soluble β-amyloid, interferes with the amyloid cascade and delays or inhibits the progression of CAA. [25]

#### **6. Summary**

**•** Cerebral amyloid angiopathy (CAA) is an important cause of spontaneous corticalsubcortical intracranial hemorrhage in the normotensive elderly.

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