Cerebral microbleeds are tiny, chronic deposits of blood in the brain that do not cause symptoms. Because an individual is unaware of their presence, they are most often discovered incidentally during a magnetic resonance imaging (MRI) scan for an unrelated reason. The presence of microbleeds is more common with advancing age and in people with certain vascular diseases.
Identifying Microbleeds with MRI Technology
The detection of cerebral microbleeds relies on specialized Magnetic Resonance Imaging (MRI) techniques sensitive to blood byproducts, as standard sequences may not visualize them. Radiologists use specific protocols that make microbleeds stand out against healthy brain tissue by detecting variations in the brain’s magnetic field.
A common technique is the T2-weighted Gradient-Recalled Echo (GRE) sequence. When red blood cells break down, they leave behind an iron-storage protein called hemosiderin. The iron in hemosiderin is paramagnetic, meaning it disrupts the local magnetic field, creating a signal loss that GRE sequences can detect.
A more sensitive technique is Susceptibility-Weighted Imaging (SWI), which uses complex data processing to enhance the contrast between hemosiderin and adjacent brain tissue. This provides a clearer depiction of microbleeds and can detect smaller lesions missed on GRE scans. On both scans, microbleeds appear as small, circular dark spots.
The sensitivity of these sequences allows for detecting blood leakage from vessels as small as 200 micrometers in diameter. Visualizing these tiny areas of past bleeding provides a detailed window into the health of the brain’s smallest blood vessels. This offers a direct look at the aftermath of minuscule hemorrhages.
Underlying Causes and Risk Factors
Cerebral microbleeds are not a disease but are a marker of underlying damage to the brain’s small blood vessels. The two most common conditions responsible for this damage are chronic hypertension (high blood pressure) and cerebral amyloid angiopathy (CAA).
Chronic hypertension exerts excessive force on the walls of the brain’s tiniest arteries. Over many years, this sustained pressure leads to a process called lipohyalinosis, where the vessel walls become thick, stiff, and brittle. This weakness makes the arteries susceptible to microscopic ruptures, resulting in leaks of blood. Microbleeds from hypertension are found in the deep structures of the brain, like the basal ganglia, thalamus, and brainstem.
Cerebral amyloid angiopathy involves the buildup of a protein called amyloid-beta within the walls of arteries in the brain. This amyloid deposition is different from the amyloid plaques seen in Alzheimer’s disease, as it specifically targets the blood vessels. The accumulation makes the vessel walls fragile and prone to bleeding, causing microbleeds located in the lobes of the brain, closer to the surface.
Therefore, the location of microbleeds on an MRI provides important clues: deep microbleeds suggest hypertensive damage, while lobar microbleeds point to CAA. Other less common factors can also lead to microbleeds, including traumatic brain injury, the effects of radiation therapy to the brain, and certain genetic disorders.
Associated Neurological Conditions and Risks
The presence of cerebral microbleeds on an MRI, while not immediately harmful, is associated with an elevated risk for future neurological events. The number and location of the microbleeds correlate with the level of risk.
Microbleeds are linked to an increased likelihood of both ischemic and hemorrhagic strokes. The same vessel fragility that causes microbleeds can lead to a larger bleed, resulting in a hemorrhagic stroke. The underlying vessel disease also impairs blood flow, increasing the risk of ischemic strokes caused by clots.
There is also a strong association between a high number of microbleeds and the development of cognitive impairment and dementia. The presence of numerous microbleeds is linked to an increased risk of developing Alzheimer’s disease and vascular dementia. This damage can disrupt communication networks between brain regions, leading to declines in cognitive functions such as processing speed, executive function, and attention.
Specifically, lobar microbleeds have been associated with a decline in memory and executive function, while deep and infratentorial microbleeds are more closely linked to deficits in attention and psychomotor speed. While the microbleeds are silent, their cumulative effect contributes to the brain damage that can manifest as cognitive decline.
Clinical Management and Monitoring
Once cerebral microbleeds are identified, there is no treatment to remove them or repair the existing damage. Clinical management focuses on controlling underlying risk factors to prevent new microbleeds and reduce the risk of future neurological events, primarily through managing cardiovascular health.
The most important intervention is strict blood pressure control. Physicians aim to maintain blood pressure below a target like 130/80 mmHg, as this reduces the risk of both stroke and dementia. This involves a combination of lifestyle modifications and antihypertensive medications.
A clinical challenge arises when a patient with microbleeds requires antithrombotic therapy, such as aspirin or warfarin, for conditions like atrial fibrillation. These medications increase the risk of bleeding. The decision to use these drugs requires weighing the patient’s risk of a clot-related event against their risk of a brain hemorrhage, a calculation influenced by the number and location of the microbleeds.
Lifestyle modifications that support vascular health are also recommended. These include:
- Adopting a healthy diet
- Engaging in regular physical activity
- Quitting smoking
- Moderating alcohol consumption
Follow-up imaging with repeat MRI scans is not routinely performed. The decision to monitor for the progression of microbleeds depends on the specific clinical context and the patient’s overall risk profile.