Symptoms and Treatments

CAA can be silent for years. Many people have amyloid deposits in their blood vessels without any noticeable signs. When symptoms do appear, they vary depending on where in the brain the disease has taken hold and whether a stroke has occurred. Not every presentation is dramatic, and this is part of what makes the condition difficult to recognize, even for clinicians. What matters most is timing.

Symptoms that are new or clearly changed within the last 24 to 48 hours may point toward acute bleeding and should be treated as an emergency. This includes sudden weakness or numbness on one side, sudden difficulty speaking or understanding speech, sudden confusion, sudden vision loss, sudden loss of balance, and a severe headache unlike any you have had before. This holds even if the symptoms are mild or have already resolved.

Symptoms that develop gradually over weeks or months are a different matter. They may not be emergencies in the way a stroke is, but they are clinically important and should be reported to your care team. Gradual changes may reflect the disease progressing, or they may have an entirely different explanation. Sorting out which requires a physician who understands CAA and can determine what evaluation, if any, is warranted.

Some people with CAA experience brief neurological episodes, sometimes called "amyloid spells." These typically begin as tingling or numbness that spreads gradually across the face, arm or hand over several minutes. Some people describe flashing or shimmering visual spots. Others have short-lived weakness or difficulty speaking. Most episodes resolve within 30 minutes, though some last longer.

These episodes are easy to mistake for a transient ischemic attack, a migraine or a seizure. That distinction matters considerably. TIAs are frequently treated with antiplatelet or anticoagulant medication, and those medications increase bleeding risk in people with CAA. Report any episode of this kind to your physician, even a brief one, and even after it has resolved.

At the slowest end of the spectrum, CAA contributes to what is known as vascular cognitive impairment. Damage builds up in the small blood vessels over years, and the effects are subtle at first: mild changes in memory, or in the mental skills used for planning, organizing and switching between tasks. These changes can happen without any obvious event, and without the person or their family connecting them to the blood vessels. This is one reason CAA is often recognized late, and one reason it is worth monitoring even in people who feel well.

MRI is the central test. Specific sequences can show microbleeds, which are small deposits of blood in the outer regions of the brain, as well as superficial siderosis, which is blood staining along the brain's surface. MRI may also show white matter changes, areas that appear altered on imaging and are common in small vessel disease of the brain.

Other conditions can cause bleeding in similar locations, including uncontrolled hypertension, vascular malformations, tumors, and the effects of anticoagulation. Additional testing may include blood work, and in some cases spinal fluid analysis, amyloid PET imaging, or genetic testing.

Diagnosis in living patients is made using the Boston criteria, a set of established standards that combine imaging findings with clinical features. Definitive confirmation requires examination of brain tissue, which is why CAA was historically confirmed only at autopsy. The Boston criteria now allow a confident diagnosis during life in most cases.

In a smaller number of people, the immune system reacts to the amyloid in the vessel walls and the surrounding brain tissue swells. Doctors call this inflammatory CAA, or CAA-related inflammation.

This form can present either way. It may arrive suddenly, with the kind of acute change described above that warrants emergency evaluation. It may also develop over weeks to months, with a gradually worsening change in thinking or behavior, new or unusual headaches, or seizures. Both presentations matter, and this form is worth recognizing because it may improve with treatment.

In some cases, inflammation is found on imaging in a person who has no symptoms at all. This does not necessarily mean treatment is needed, but it does change how closely the condition is monitored.

CAA increases the risk of bleeding in the brain, and blood thinning medications, including anticoagulants and antiplatelet drugs, add to that risk. But the picture is more complicated than it first appears. Although CAA is recognized through bleeding events, people with CAA also carry a substantial risk of clot-related problems: narrowed arteries, heart disease, and ischemic stroke, the kind caused by a blocked vessel rather than a bleed. Both risks are real, and in many patients they compete directly.

Sorting out that balance requires looking at each case individually. Bleeding risk is assessed through MRI findings and clinical history. Clot-related risk is assessed separately. Some cases are genuinely difficult, with strong arguments on both sides, and high-quality trial data to guide these decisions remains limited.

This is one of the central questions we address in the CAA Clinic: whether a particular person should be on a blood thinner, and at what blood pressure targets we should be aiming. Do not start or stop any of these medications on your own. Talk with your healthcare team, and we may be able to offer additional insight into whether these medications are appropriate in your specific situation.

Controlling blood pressure is one of the most important steps a person with CAA can take. High blood pressure puts additional stress on already-weakened vessel walls, raising the risk of rupture. Your care team will work with you to reach your targets through medication, diet and lifestyle changes.

When a brain bleed does occur, treatment depends on the size and location of the hemorrhage and the patient's overall condition. Some bleeds are managed with close monitoring in a hospital setting. Others may require surgical intervention to relieve pressure on the brain. A neurology or neurosurgery team will determine the appropriate course of action based on each individual case.

When inflammation is the driver, treatment differs from the rest of CAA care. Corticosteroids or other medications that suppress the immune response may reduce the swelling, and some people improve substantially. Treatment decisions depend on how the condition presents and how it responds, and they require close monitoring with repeat imaging.

Because CAA is associated with cognitive decline, addressing brain health broadly is an important part of care. Regular physical activity, social engagement, a heart-healthy diet and adequate sleep all support brain function over time. These are not cures, but they give the brain the best possible conditions to stay resilient.

Medication may be prescribed to help manage specific cognitive symptoms, particularly if CAA occurs alongside Alzheimer's disease or another form of dementia.

Certain symptoms require immediate emergency attention. Call 911 right away if you or someone around you experiences:

• A sudden, severe headache unlike any before
• Sudden weakness or numbness in the face, arm or leg
• Sudden difficulty speaking, understanding speech or finding words
• Sudden loss of vision
• Sudden loss of balance or coordination
• Confusion or unusual behavior that comes on quickly

These could be signs of an acute brain bleed. Time is critical. The faster a person receives care, the better the chance of limiting brain damage and supporting recovery.

If you have already been diagnosed with CAA and notice gradual changes in memory, thinking or daily functioning, schedule an appointment with the Ochsner CAA Clinic. These changes deserve evaluation even if they are not accompanied by sudden symptoms.