Cerebral amyloid angiopathy is a brain blood-vessel problem. In CAA, tiny proteins called amyloid-beta (Aβ) build up in the walls of small and medium arteries on the surface of the brain and in the outer layers of the brain. Over time, these vessel walls become weak and fragile. When a fragile brain vessel leaks or bursts, bleeding can happen in the brain’s outer “lobar” areas. CAA is common as people get older and is a major cause of spontaneous brain bleeds that are not due to high blood pressure. CAA can also be linked to thinking problems, brief stroke-like spells, small “silent” bleeds, and changes seen on brain scans. PMCAmerican Heart Association Journals
Cerebral amyloid angiopathy (CAA) is a condition where a sticky protein called amyloid-beta builds up in the walls of small blood vessels on the surface and in the outer parts (lobes) of the brain. Over time, these vessels become fragile and leaky, so people with CAA are at higher risk of bleeding on the brain (especially in the lobes), tiny “microbleeds,” and a specific kind of thin bleeding over the brain surface called convexity subarachnoid hemorrhage. CAA can also cause brief, spreading “amyloid spells” (short episodes of tingling, weakness, or visual symptoms), headaches, and sometimes problems with thinking and memory. There is no cure yet, but careful day-to-day management can lower complications and help you live more safely. NCBIPMC+1
CAA is a problem where protein deposits make brain vessels brittle, and brittle vessels are more likely to ooze or bleed, especially in the outer parts of the brain (the lobes). That is why people with CAA often have small brain bleeds on MRI or larger bleeds that cause sudden symptoms. PMC
Doctors rarely need a brain biopsy to diagnose CAA. Instead, they use your story, your age (usually 50 or older), your symptoms (like a lobar brain bleed, brief spreading numbness spells, or cognitive decline), and very specific MRI features. These features include multiple strictly lobar microbleeds, thin “stains” of old blood on the surface called cortical superficial siderosis, and other supportive markers. The updated Boston Criteria version 2.0 (released in 2022 and validated since) improved accuracy by adding newer MRI markers. In short: if your symptoms and MRI match these patterns, you can be diagnosed with “probable CAA” without surgery. PMC+1American Academy of Neurology
A few MRI findings that strongly point to CAA include lobar microbleeds, cortical superficial siderosis, and sometimes convexity subarachnoid hemorrhage (a thin layer of blood over the brain surface), plus white-matter change patterns and enlarged perivascular spaces in certain brain regions. These patterns are core to Boston Criteria v2.0. SpringerLinkMDPI
Types of CAA
Sporadic CAA (the common type).
This is the typical, age-related form. It happens as we get older, often alongside or independent of Alzheimer-type changes. It mostly involves Aβ protein in brain vessel walls. PMCHereditary (familial) CAA (rare, runs in families).
Some families carry gene changes that cause early or severe CAA. Examples include APP “Dutch” type, APP “Iowa/Arctic/Flemish” variants, cystatin C (Icelandic type), and ITM2B (British/Danish types). These forms tend to start younger and bleed more. PMCOxford AcademicInflammatory CAA (CAA-ri) and Aβ-related angiitis (ABRA).
In a subset, the immune system reacts to vessel amyloid and causes vasogenic swelling (edema) around affected vessels. Symptoms often come on subacutely with headaches, seizures, confusion, or focal deficits, and they often improve with steroids or other immunosuppressants. Think of this as “CAA plus inflammation.” JAMA NetworkPMCIatrogenic (treatment-related) CAA (very rare).
A few people exposed in childhood to certain cadaveric tissue products (for example, old dura grafts or growth hormone preparations) can develop early-onset CAA decades later, likely due to prion-like seeding of Aβ. PMCjnnp.bmj.comPathology distribution types (Type 1 vs Type 2).
Pathologists also describe CAA as Type 1 (capillary involvement) or Type 2 (no capillaries, mainly leptomeningeal/cortical arteries). This split helps research and sometimes correlates with imaging and genetics. PubMedOxford Academic
Causes
CAA itself is caused by amyloid-beta depositing in brain vessel walls. Below are simple, concrete factors that cause, drive, worsen, or trigger complications of CAA.
Aging.
Older age slows amyloid clearance and raises Aβ in vessel walls, so vessels grow fragile over time. PMCApolipoprotein E (APOE) genes ε2 and ε4.
These common genetic variants increase amyloid build-up in vessel walls and raise the chance of lobar hemorrhage and its recurrence. JAMA NetworkPMCGeneral amyloid-beta overproduction or poor clearance.
When the brain produces more Aβ or clears it poorly, more deposits form in vessel walls. PMCAPP gene mutations (hereditary CAA).
Specific changes in the APP gene (for example, Dutch/Iowa/Arctic variants) directly drive early and severe amyloid vessel disease. PMCCystatin C (CST3) mutation (Icelandic type).
This rare genetic cause produces a different amyloid (cystatin C) in vessel walls, leading to early brain bleeding. PMCITM2B (BRI2) gene mutations (British and Danish types).
These rare familial disorders cause amyloid build-up in brain vessels with early symptoms. Oxford AcademicDown syndrome (extra copy of APP).
Extra APP in Down syndrome increases brain amyloid; CAA is common although major bleeding is less frequent than in sporadic CAA. PMCNatureIatrogenic exposure to amyloid seeds (historical tissue products).
Rare past exposures (e.g., some cadaveric dura or growth hormone) can “seed” Aβ that later causes CAA. PMCPrior lobar intracerebral hemorrhage.
A previous lobar bleed suggests underlying CAA and raises the chance of another, especially with certain APOE genotypes. PubMedCortical superficial siderosis (cSS).
This MRI sign of old superficial bleeding marks fragile surface vessels and predicts future bleeds. Oxford AcademicAnticoagulant medicines (blood thinners).
These drugs don’t cause CAA, but they raise the risk and severity of bleeding in people who already have fragile CAA vessels. PMCJACCAntiplatelet medicines.
These also don’t cause CAA, but they are linked to more lobar microbleeds and can raise the risk of symptomatic bleeds in CAA. PMCAmyloid-modifying antibody treatments (ARIA risk).
Anti-amyloid monoclonal antibodies (used for Alzheimer’s disease) can cause ARIA-E (edema) or ARIA-H (microbleeds), especially in people with CAA markers or APOE-ε4. PMC+1CAA-related inflammation (CAA-ri).
An autoimmune reaction to vessel amyloid can acutely weaken vessels and trigger edema and bleeding. PMCPerivascular drainage failure with aging.
As waste-clearance pathways around vessels slow with age, amyloid builds up more easily in vessel walls. (This is a widely accepted mechanism in CAA research.) PMCCerebral small-vessel disease changes.
Other age-related vessel changes can coexist and make bleeding more likely once amyloid is present. Journal of StrokeHypertension as a co-factor.
High blood pressure is not the classic cause of lobar bleeds (that’s CAA), but it can still stress fragile amyloid-laden vessels and worsen outcomes. ScienceDirectTraumatic brain injury (possible long-term link).
Some evidence suggests trauma can speed amyloid buildup and vascular amyloid changes over time. The LancetAPP duplication/over-dosage outside classic DS.
Duplicating the APP gene (even without full Down syndrome) boosts amyloid and is linked with CAA. Alzheimer’s JournalsAPOE-ε2-specific vessel effects.
Beyond general risk, ε2 seems tied to vessel wall tearing and hematoma expansion in lobar bleeds. American Heart Association Journals
Symptoms and signs
Sudden weakness or numbness on one side.
A lobar bleed can damage the opposite side of the body’s movement or sensation.Sudden trouble speaking or understanding.
Bleeds in language areas cause slurred speech, word-finding trouble, or trouble understanding.Vision loss or “blind spots.”
Occipital lobe involvement can take out a chunk of your visual field.Brief spreading tingling, weakness, or visual zigzags (TFNEs).
These transient focal neurological episodes often come from tiny surface bleeds and cortical superficial siderosis; they usually last minutes. Oxford AcademicSevere headache (sometimes sudden).
Surface bleeding or convexity subarachnoid blood can cause a sudden, intense headache.Confusion or sudden personality change.
A new lobar bleed or active inflammation can change thinking or behavior for days to weeks.Seizures.
Blood irritating the cortex can trigger seizures shortly after a bleed, or later.Memory and thinking problems over time.
Repeated microbleeds, white-matter damage, or coexisting Alzheimer changes can quietly reduce memory and processing speed. PMCGait imbalance or clumsiness.
Bleeds or microbleeds in motor pathways cause unsteady walking or poor coordination.Dizziness or vertigo.
Acute bleeding can upset balance networks and cause spinning or lightheadedness.Nausea and vomiting.
A fresh bleed raises pressure and can trigger vomiting.Drowsiness or reduced alertness.
Large bleeds or swelling can make you very sleepy.Loss of consciousness (in big bleeds).
A large lobar hemorrhage can briefly knock you out.Mood changes (anxiety, depression, apathy).
Chronic microvascular injury and repeated small bleeds can affect mood and motivation.Headache plus focal symptoms that come and go (CAA-ri).
Inflammatory CAA often brings headaches, seizures, and waxing-waning deficits that improve with steroids. JAMA Network
Diagnostic tests
A) Physical exam (bedside, no machines)
General neurological exam.
The doctor checks strength, sensation, reflexes, eye movements, speech, and coordination to map what part of the brain is affected right now.Vital signs and cardiovascular exam.
Blood pressure, pulse, and heart rhythm are checked because high BP or abnormal rhythms change stroke risk and rescue decisions.Level of consciousness check.
Simple questions and responses show if a bleed or swelling is making you drowsy or confused.Cranial nerve and visual field testing.
Finger counting and face-tracking can reveal vision cuts or eye movement problems from lobar lesions.Gait and balance testing.
Standing, walking, heel-to-toe, and turning tests show coordination and cerebellar involvement.
B) “Manual” bedside tests (quick, hands-on assessments)
NIH Stroke Scale scoring.
A structured checklist grades stroke severity and tracks change over time.Bedside cognitive screening (MoCA or MMSE).
Short memory-attention tests help spot thinking problems that can occur with CAA.Language tasks (naming, repetition, following commands).
Simple tasks pinpoint language-area involvement from a lobar bleed.Coordination maneuvers (finger-to-nose, heel-to-shin).
These show whether pathways that control smooth movement are affected.Sensory and neglect checks.
Light-touch and double-simultaneous stimulation can uncover neglect or sensory loss common with lobar injuries.
C) Laboratory and pathological tests
Complete blood count (CBC).
Checks anemia or low platelets that can worsen bleeding.Clotting studies (PT/INR, aPTT).
Reveals if anticoagulants or a clotting problem are present, which strongly affects management and bleeding risk. ScienceDirectKidney and liver function.
These help decide on imaging contrast safety and medication choices.Inflammation labs (ESR/CRP) if CAA-ri suspected.
These are nonspecific but help support an inflammatory picture.Cerebrospinal fluid (CSF) analysis if CAA-ri is suspected.
A lumbar puncture may show high protein and mild white-cell increase (and usually no oligoclonal bands), which support an inflammatory form of CAA. PMC+1Genetic testing when hereditary CAA is likely.
If there is early onset or a strong family pattern, testing for APP, CST3, or ITM2B mutations may confirm a familial CAA type. PMCBrain tissue pathology (biopsy or autopsy).
This is the gold standard but is rarely needed. Congo-red staining and special antibodies show amyloid in vessel walls. (Most living diagnoses rely on MRI patterns instead.) American Heart Association Journals
D) Electrodiagnostic test
EEG (electroencephalogram).
This looks for seizure activity that can accompany lobar bleeding, microbleeds, or inflammatory CAA.
E) Imaging tests (core to diagnosis)
Non-contrast head CT (first-line in emergencies).
Fast and excellent for detecting an acute hemorrhage in the lobes.MRI brain with advanced sequences (the cornerstone).
T2-GRE or Susceptibility-Weighted Imaging (SWI):* shows microbleeds and cortical superficial siderosis typical of CAA.
FLAIR: shows convexity subarachnoid blood, white-matter changes, and vasogenic edema in inflammatory CAA.
Diffusion-weighted imaging (DWI): detects small acute infarcts that sometimes occur in CAA.
These features together form the Boston Criteria v2.0 map for “probable CAA.” PMCSpringerLink
Non-pharmacological treatments
None of these “treat” the amyloid itself. They lower your risk of bleeding, protect the brain, and help daily life. Each includes a short description, purpose, and “how it helps.”
Tight, steady blood-pressure control
Purpose: Cut the risk of new bleeds.
How it helps: High or swinging blood pressure stretches fragile vessels. Doctors aim for smooth, sustained control and avoid big ups and downs. Home BP logs help. cpr.heart.orgRapid stroke-care plan
Purpose: Get urgent help if symptoms start (sudden weakness, speech problems, severe headache).
How it helps: Fast emergency care improves survival and function after brain bleeds. American Heart Association JournalsFall-prevention and home safety
Purpose: Prevent head injury that could trigger bleeding.
How it helps: Remove trip hazards, add grab bars, use night lights, check shoes, and consider a cane/walker if balance is poor.Balance & strength training (physiotherapy)
Purpose: Reduce falls, keep mobility.
How it helps: Leg and core exercises, tai chi-style balance work, and supervised gait training lower fall risk.Occupational therapy
Purpose: Make daily activities safer and easier.
How it helps: Adapts your home, bathroom, and kitchen; teaches safer transfer and dressing methods.Sleep apnea screening and treatment (e.g., CPAP if indicated)
Purpose: Protect brain vessels by reducing nighttime BP surges and low oxygen.
How it helps: Treating apnea supports steadier blood pressure and brain health.Headache hygiene
Purpose: Limit triggers of CAA-related headaches and “amyloid spells.”
How it helps: Regular sleep, hydration, caffeine consistency, and stress control may reduce symptom flares.Cognitive rehabilitation
Purpose: Support attention, memory, and planning.
How it helps: Structured exercises and compensatory strategies (notes, alarms, routines) help daily function.Medication “brown-bag” review
Purpose: Find drugs that increase bleeding risk or cause dizziness/falls.
How it helps: Your clinician may adjust antithrombotics (blood thinners/antiplatelets), sedatives, or blood-pressure meds to safer choices in CAA. PMCThe LancetStroke-savvy nutrition (Mediterranean/DASH/MIND eating patterns)
Purpose: Support blood-vessel health and steady BP.
How it helps: More vegetables, fruits, whole grains, legumes, nuts, olive oil, and fish; less salt, sugar, and processed food. These patterns are linked with lower stroke risk and slower cognitive decline. PMCNHLBI, NIHPubMedSodium reduction
Purpose: Lower BP safely.
How it helps: Aim for ~1,500–2,300 mg sodium/day (your doctor may tailor this). www.heart.orgNHLBI, NIHRegular aerobic activity (as safe for you)
Purpose: Support BP, mood, cognition, and balance.
How it helps: Walking most days, gentle cycling, or water aerobics; start low, go slow, and use a fall-safe plan.Alcohol moderation and smoking cessation
Purpose: Reduce vessel injury and BP spikes.
How it helps: No tobacco; limit alcohol to low-risk amounts per your clinician.Hydration and constipation prevention
Purpose: Avoid BP swings and straining.
How it helps: Regular fluids and fiber soften stools and reduce spikes in intracranial pressure from straining.Vision and hearing checks
Purpose: Reduce falls and isolation.
How it helps: Correcting vision/hearing supports balance, attention, and social engagement.Stress reduction & mental health care
Purpose: Lower BP variability and improve quality of life.
How it helps: Breathing techniques, mindfulness, counseling, and caregiver support groups.Seizure-smart living
Purpose: Safety if a seizure occurs.
How it helps: Shower chair, avoid heights/open water alone; loved ones learn basic seizure first aid. (Medicine details below.)Plan for “amyloid spells” (TFNEs)
Purpose: Recognize brief sensory/visual episodes and act wisely.
How it helps: These are often bleeding-related, not TIAs, and may signal higher hemorrhage risk; alert clinicians, avoid self-starting antiplatelets for new spells without medical advice. PMCPubMedMedical alert info
Purpose: Inform emergency teams you have CAA.
How it helps: Guides decisions on blood thinners, reversal agents, and surgery.Shared decision-making about blood thinners/antiplatelets
Purpose: Balance stroke-clot risks vs. brain-bleed risks for you.
How it helps: Decisions for atrial fibrillation or heart stents are individualized; in some cases left atrial appendage occlusion may be considered when anticoagulants are too risky. PMC
Evidence-based drug treatments
There is no proven, disease-modifying drug for sporadic CAA yet. Medicines below treat complications (bleeding, seizures, CAA-related inflammation) or reduce risk. Doses are typical adult ranges—your team individualizes them.
Aggressive BP-lowering in acute brain bleed (e.g., IV nicardipine infusion 5 mg/h up-titrated; or IV labetalol 10–20 mg boluses)
Purpose: Limit hematoma growth.
Mechanism: Smooth, sustained BP control lowers pressure on fragile vessels.
Side effects: Low BP, slow heart rate (labetalol), headache, flushing (nicardipine). American Heart Association Journalscpr.heart.orgReversal of blood thinners during bleeding
• PCC (4-factor prothrombin complex concentrate) for warfarin; idarucizumab for dabigatran; andexanet alfa or PCC for factor Xa inhibitors, per local protocol.
Purpose: Stop active bleeding quickly.
Mechanism: Replenish clotting or neutralize the drug.
Key caution: Timing and choice depend on the specific anticoagulant. American Heart Association JournalsSeizure treatment when seizures occur (e.g., levetiracetam 500–1,500 mg twice daily; alternatives by clinician)
Purpose: Prevent recurrent seizures after CAA-related bleeds.
Mechanism: Stabilizes neuronal activity.
Notes: Routine prophylaxis after ICH is generally not recommended; treat if seizures happen or risk is high.
Side effects: Sleepiness, mood changes. PMCSteroids for CAA-related inflammation (CAA-ri) (e.g., IV methylprednisolone 500–1,000 mg/day for 3–5 days, then oral taper)
Purpose: Calm vessel wall inflammation that flares around amyloid deposits.
Mechanism: Immune suppression reduces edema and symptoms.
Side effects: High blood sugar, infection risk, mood changes. PMCJAMA NetworkSecond-line immunosuppressants for steroid-refractory CAA-ri (e.g., cyclophosphamide, mycophenolate mofetil, rituximab, IVIG, tailored by specialists)
Purpose: Control ongoing inflammation when steroids alone are not enough.
Mechanism: Reduce abnormal immune activity.
Side effects: Bone-marrow suppression, infection risk, nausea—specialist monitoring needed. JAMA Networkjns-journal.comCareful, individualized use of antiplatelet therapy after a prior ICH only when the benefit outweighs risk (e.g., essential cardiac indications)
Purpose: Prevent clots where strongly indicated.
Mechanism: Platelet inhibition.
Evidence note: In some survivors of ICH, restarting antiplatelets did not increase recurrent ICH in trials like RESTART, but decisions in CAA are highly individualized.
Risks: More microbleeds and bleeding with higher lobar burden. PMCAmerican Heart Association JournalsAnticoagulation decisions in atrial fibrillation + CAA
Purpose: Prevent cardioembolic stroke vs. avoid brain hemorrhage.
Mechanism: Thrombin/Xa inhibition (warfarin/DOACs).
Evidence note: Data are evolving; some reviews propose risk-based, shared decisions and in select cases left atrial appendage occlusion instead of long-term anticoagulation.
Risks: Lobar ICH risk is high in CAA; therapy choice is case-by-case. PMCThe LancetHeadache management (e.g., acetaminophen as first-line; avoid NSAIDs unless your doctor approves)
Purpose: Relieve pain without raising bleeding risk.
Mechanism: Central analgesia (acetaminophen).
Side effects: Liver toxicity at high doses—stay within safe daily limits; check all combination products.Depression/anxiety treatment (e.g., SSRIs/SNRIs when appropriate)
Purpose: Improve mood, sleep, and participation in rehab.
Mechanism: Neurotransmitter modulation.
Notes: Some SSRIs have been linked to bleeding risk; prescribers balance pros/cons carefully in CAA.Cholesterol and vascular risk management (e.g., statins if otherwise indicated)
Purpose: Treat overall vascular risk profile.
Mechanism: Lipid lowering, pleiotropic vascular effects.
Notes: Statins aren’t a CAA treatment; your clinician individualizes use after ICH.
Dietary molecular supplements
No supplement has been proven to treat CAA. These are general “brain- and vessel-friendly” nutrients discussed with your clinician, especially if you are deficient. Evidence strength varies.
Omega-3 fatty acids (EPA/DHA) – typical food-first approach; if supplementing, common doses are 1–2 g/day total EPA+DHA (or prescription EPA when indicated).
Function/Mechanism: Anti-inflammatory lipid mediators; support vascular health.
Notes: Higher omega-3 levels relate to lower ischemic stroke risk, not proven for hemorrhagic stroke; high-dose oils may raise atrial-fibrillation risk in some settings—discuss with your doctor. American Heart Association Journals+1Vitamin D – dose per blood level (often 1,000–2,000 IU/day, individualized).
Function: Neuro-immune and vascular signaling; deficiency is common.
Mechanism/Evidence: Low vitamin D is linked to higher stroke risk and worse prognosis; supplementing aims to correct deficiency. PMCB-vitamins (B6, B12, folate) – doses vary (e.g., B12 500–1,000 mcg/day, folate 400–800 mcg/day).
Function: Lower homocysteine; support myelin and neuronal metabolism.
Mechanism/Evidence: In MCI, B-vitamins slowed brain atrophy when homocysteine was high. PMCMagnesium – 200–400 mg/day (as citrate/glycinate; adjust for kidneys).
Function: BP, neuromuscular stability.
Mechanism: Vascular tone and neurotransmission support.Potassium (dietary focus) – from foods (leafy greens, beans, bananas) per kidney status.
Function: BP control.
Mechanism: Counterbalances sodium to steady BP.Polyphenols (berries, cocoa, green tea)
Function: Antioxidant/anti-inflammatory compounds.
Mechanism: May support endothelial function and cognition; food sources preferred.Curcumin (from turmeric) – standardized extracts often 500–1,000 mg/day with piperine; discuss drug interactions.
Function: Anti-inflammatory; lab data suggest anti-amyloid aggregation, but clinical evidence remains limited.Coenzyme Q10 – 100–200 mg/day with fat-containing meal.
Function: Mitochondrial support; antioxidant.Probiotics/fermented foods
Function: Gut-brain axis support, possibly blood-pressure effects.L-citrulline or beetroot (nitrate source)
Function: Nitric-oxide pathway support for vascular tone.
Note: May alter BP; clinician guidance is vital.
Immune/regenerative” drugs
For CAA-related inflammation (CAA-ri), doctors use immunosuppressive medicines. There are no approved stem-cell or regenerative drugs for CAA today.
IV methylprednisolone (see dose above) → Purpose/Mechanism: Rapid immune suppression to settle vessel-wall inflammation; often first-line. PMC
Oral prednisone taper → Purpose: Maintain remission after IV pulse; Mechanism: Ongoing immune dampening. PMC
Cyclophosphamide (specialist-dosed) → Purpose: Steroid-refractory disease; Mechanism: Broad immune-cell suppression. jns-journal.com
Mycophenolate mofetil → Purpose: Steroid-sparing; Mechanism: Inhibits lymphocyte purine synthesis. JAMA Network
Rituximab → Purpose: Selected refractory cases; Mechanism: B-cell depletion. JAMA Network
IVIG (intravenous immunoglobulin) → Purpose: Immune modulation in select cases; Mechanism: Complex antibody-mediated immune effects. JAMA Network
About regenerative/stem-cell approaches: Some labs and early clinical research explore neurovascular repair strategies for brain hemorrhage and Alzheimer’s disease, but no stem-cell therapy is approved for CAA. If you see such offers, treat them as experimental and discuss clinical-trial options with your neurologist. (General research context; no specific CAA approval yet.)
Surgeries/procedures
Surgical evacuation of a lobar hematoma (open craniotomy or minimally invasive techniques)
Why: In selected patients with large, accessible lobar bleeds causing pressure or decline, removing the clot can reduce mass effect. Selection is strict and individualized. www.heart.orgMinimally invasive ICH evacuation (stereotactic catheter ± thrombolysis, or endoscopic)
Why: For some supratentorial bleeds, minimally invasive approaches may reduce mortality or improve outcomes compared with medical care alone in carefully chosen cases. Evidence continues to evolve. www.heart.orgExternal ventricular drain (EVD) for intraventricular hemorrhage with hydrocephalus
Why: To relieve dangerous fluid buildup and lower pressure; sometimes combined with endoscopic clot removal or intraventricular thrombolysis. www.heart.orgDecompressive hemicraniectomy
Why: In life-threatening swelling from a large bleed, temporarily removing part of the skull reduces pressure and prevents herniation in selected cases. www.heart.orgLeft atrial appendage occlusion (for AF when anticoagulation is too risky)
Why: In people with AF and very high hemorrhage risk (e.g., CAA), this heart procedure reduces clot risk without long-term full-dose anticoagulation. Decisions are multidisciplinary. PMC
Prevention priorities
Keep blood pressure steady and in your target range. cpr.heart.org
Do not start or stop blood thinners/antiplatelets on your own; always discuss with your clinician. PMC
Practice fall prevention and protect your head.
Treat sleep apnea if present.
Follow a Mediterranean/DASH/MIND eating pattern; limit salt. PMCNHLBI, NIH
Don’t smoke; keep alcohol low.
Stay physically active with a fall-safe plan.
Keep diabetes, cholesterol, and weight in healthy ranges.
Stay up-to-date on vision/hearing and medication reviews.
Learn to recognize TFNEs (“amyloid spells”) and seek medical advice promptly. PMC
When to see a doctor now
Sudden weakness, numbness, trouble speaking, confusion, severe headache, vision loss, or collapse.
New or changing brief spreading tingling/weakness or visual zig-zags (possible TFNEs). PMC
New seizures, fainting, repeated falls, or a strong hit to the head.
Worsening headache, sleepiness, vomiting, or any new neurologic symptom.
What to eat—and what to avoid
Eat more of:
Vegetables & leafy greens (every meal if possible).
Berries (polyphenols for brain health).
Legumes & whole grains (fiber for BP and gut health).
Nuts & seeds (a small handful daily).
Olive oil as main fat.
Fish (especially oily fish 1–2×/week).
Yogurt/fermented foods (if tolerated).
Potassium-rich foods (beans, bananas, pumpkin, spinach).
Adequate water (unless fluid-restricted).
Small portions of dark chocolate (high-cocoa, low sugar).
Limit/avoid:
High-salt foods (chips, instant noodles, processed meats). www.heart.org
Ultra-processed snacks & sweets.
Trans fats and large amounts of saturated fat.
Sugar-sweetened beverages.
Binge alcohol; keep intake low.
High-dose fish-oil supplements without medical advice (possible AF risk at higher doses). American Heart Association Journals
Energy drinks and excessive caffeine if they spike BP.
Licorice (can raise BP).
Very low-carb crash diets that destabilize BP or cause dehydration.
Any supplement stacks without checking for drug interactions.
Frequently asked questions
Is CAA the same as Alzheimer’s disease (AD)?
No. They share amyloid-beta, but CAA affects vessel walls while AD affects brain tissue (plaques/tangles). Many people can have both. PMCHow is CAA diagnosed without a biopsy?
With the Boston Criteria v2.0, which use MRI markers (lobar microbleeds, cortical superficial siderosis, certain white-matter changes) plus clinical features to label “probable CAA.” PMCWhat are “amyloid spells”?
Short, spreading sensory/visual or motor episodes (TFNEs). They often relate to tiny surface bleeds, not ischemic TIAs, and predict higher ICH risk—so call your doctor. PMCCan CAA be cured?
Not yet. Today’s care prevents complications and supports life quality. Research into disease-modifying therapies is ongoing. MDPIWill I always bleed again?
Not always, but risk is higher than average. Good BP control, fall prevention, and careful decisions about antithrombotics help reduce risk. cpr.heart.orgCan I take aspirin or blood thinners?
Only if the benefit clearly outweighs the bleeding risk, after a detailed discussion with your team. In AF, device-based left atrial appendage occlusion may be an option if anticoagulation is too risky. PMCDo I need seizure medication?
Only if you have a seizure or your doctor sees a strong reason. Routine prevention after ICH is generally not recommended. PMCWhat is CAA-related inflammation (CAA-ri)?
An immune flare around amyloid in vessel walls that causes headaches, confusion, or focal deficits; it often responds to steroids and sometimes other immunosuppressants. PMCAre anti-amyloid Alzheimer’s drugs used for CAA?
They are not approved for CAA and can increase brain-bleed risk in people with cerebral amyloid. Your specialist will weigh risks very carefully.Is surgery always needed for a bleed?
No. Many bleeds are managed medically. Surgery is considered for selected large, accessible lobar bleeds, severe swelling, or hydrocephalus. www.heart.orgShould I avoid MRI?
MRI is a key tool for diagnosing and monitoring CAA; it is safe for most people (check for implants). PMCIs CAA genetic?
Most cases are sporadic and age-related. Rare inherited forms exist; your team will tell you if testing makes sense. PMCCan I travel?
Often yes—plan for medications, hydration, movement during long trips, and quick access to emergency care.What about diet and supplements?
Food-first patterns (Mediterranean/DASH/MIND) and correcting proven deficiencies (vitamin D/B-vitamins) support overall vascular and cognitive health; no supplement treats CAA. PMCPubMedWhat should caregivers know?
Learn stroke warning signs, create a fall-safe home, help with meds, and watch for new spells, headaches, confusion, or weakness.
Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.
The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: August 15, 2025.
