In an 82-year-old woman with mild dementia presenting with acute right-sided weakness, confusion, and MRI showing lobar microbleeds in the left parietal, frontal, and cerebellar regions, which is the most likely diagnosis: infectious vasculitis, hypertensive arteriopathy, cerebral venous sinus thrombosis, or cerebral microangiopathy?

Cerebral Amyloid Angiopathy (CAA)

The most likely diagnosis in this 82-year-old woman with lobar microbleeds in multiple locations (left parietal, frontal, and cerebellar regions) is cerebral amyloid angiopathy (CAA), which represents the underlying microangiopathy causing her acute stroke presentation.

Clinical Reasoning

Why CAA is the Primary Diagnosis

• Lobar microbleed distribution is pathognomonic for CAA rather than hypertensive arteriopathy, which typically causes deep (basal ganglia, thalamus) and infratentorial microbleeds 1, 2
• The patient's microbleeds are located in cortical/lobar regions (parietal, frontal, cerebellar cortex), which strongly suggests amyloid deposition in leptomeningeal and cortical vessels rather than deep perforating arteries 1
• At 82 years of age with pre-existing dementia, CAA is extremely common and represents deposition of amyloid-β protein in the walls of small to medium-sized cerebral arteries 1
• The presence of microbleeds in multiple lobar locations (left parietal, frontal, and cerebellar) indicates widespread CAA affecting cortical vessels 2, 3

Why Other Diagnoses Are Less Likely

Hypertensive arteriopathy (Option B):

• Would produce microbleeds predominantly in deep structures (basal ganglia, thalamus, pons) and deep white matter, not lobar cortical regions 2, 3
• While the patient has mild hypertension (BP 152/86), the lobar distribution of microbleeds argues against pure hypertensive vasculopathy 1, 2
• Hypertensive microbleeds are typically infratentorial and in deep gray matter, not in cortical lobar locations 3

Infectious vasculitis (Option A):

• Would present with systemic signs of infection (fever, elevated inflammatory markers, CSF pleocytosis), which are not described 1
• Vasculitis typically causes enhancement on MRI and acute inflammatory changes, not chronic microbleeds 1
• The chronic nature of microbleeds and absence of acute inflammatory features makes this diagnosis unlikely 1

Cerebral venous sinus thrombosis (Option C):

• Presents with venous infarcts that are hemorrhagic, edematous, and do not respect arterial territories 1
• Would show venous engorgement, cord sign, or empty delta sign on imaging 1
• The pattern of small punctate microbleeds in arterial territories is inconsistent with venous thrombosis 1

Clinical Implications and Management Considerations

Immediate Management Priorities

• Avoid anticoagulation and aggressive antiplatelet therapy in patients with lobar microbleeds due to high risk of intracerebral hemorrhage from underlying CAA 1
• The presence of lobar microbleeds on MRI increases the risk of ICH to 9.3% in anticoagulated patients compared to 1.3% without microbleeds 1
• Blood pressure should be controlled but not aggressively lowered in the acute stroke setting, maintaining permissive hypertension initially 1, 4

Prognostic Considerations

• Multiple lobar microbleeds significantly increase dementia risk (HR 1.74 for any CMB, HR 2.99 for deep and mixed CMB) 3
• Patients with CAA and microbleeds show worse performance on cognitive tests, particularly in psychomotor speed and executive functioning 5
• The combination of pre-existing dementia and new lobar microbleeds suggests progressive CAA with high risk of recurrent hemorrhagic events 5, 2

Long-term Management Strategy

• Target systolic blood pressure <140 mmHg (not <120 mmHg as in pure ischemic disease) to balance stroke prevention against hemorrhage risk in CAA 1, 4
• Consider aspirin 75-81 mg daily for secondary stroke prevention, but weigh carefully against hemorrhage risk given multiple lobar microbleeds 1, 4
• Avoid warfarin or other anticoagulants even for compelling indications like atrial fibrillation, as lobar ICH risk is prohibitively high 1
• Serial MRI monitoring every 2-3 years to assess progression of microbleeds and white matter disease 4

Critical Pitfall to Avoid

Do not assume this is simply "hypertensive arteriopathy" based on age and mild hypertension alone—the lobar distribution of microbleeds is the critical distinguishing feature that identifies CAA as the underlying pathology 2, 3. This distinction is essential because CAA carries much higher hemorrhage risk with antithrombotic therapy compared to hypertensive microangiopathy 1.