Cerebral Amyloid Angiopathy
The most likely explanation for this elderly woman's findings is cerebral amyloid angiopathy (CAA), given the combination of lobar microbleeds in multiple cortical locations, pre-existing mild dementia, and her age. 1
Key Diagnostic Features Supporting CAA
The distribution pattern of microbleeds is the critical distinguishing feature. The patient has microbleeds in the left parietal lobe, frontal lobe, and left cerebellum—predominantly lobar (cortical) locations. 2
- Lobar microbleeds are highly specific for CAA, representing chronic hemorrhagic lesions from β-amyloid deposition in cortical vessel walls 2, 1
- Multiple juxtacortical microhemorrhages on MRI are pathognomonic for CAA rather than hypertensive arteriopathy 1, 3
- CAA characteristically affects cortical and leptomeningeal vessels, producing lobar hemorrhages and microbleeds 2
Why Not Hypertensive Arteriopathy
Hypertensive arteriopathy produces a distinctly different pattern of microbleeds. 2, 4
- Hypertensive microbleeds occur in deep structures: basal ganglia, thalamus, pons, and deep white matter—not predominantly lobar locations 2, 1, 4
- While this patient has mild hypertension (BP 152/86), the lobar distribution of her microbleeds argues against hypertensive arteriopathy as the primary etiology 2, 5
- The presence of pre-existing dementia further supports CAA, as hypertensive arteriopathy typically presents with vascular cognitive impairment and stepwise decline rather than progressive dementia 2
Clinical Context Strengthening CAA Diagnosis
The patient's clinical profile aligns with typical CAA presentation. 2, 5
- Elderly age is the strongest risk factor for CAA 2
- Pre-existing mild dementia is commonly associated with CAA due to shared β-amyloid pathophysiology 1, 5
- Recent TIA followed by acute stroke symptoms reflects the hemorrhagic tendency of weakened CAA vessels 2
- CAA frequently coexists with Alzheimer's disease pathology, both involving β-amyloid deposition 5, 4
Ruling Out Other Diagnoses
Infectious vasculitis would present with systemic signs (fever, elevated inflammatory markers), CSF pleocytosis, and vessel wall enhancement on MRI—none of which are described here 2
Cerebral venous sinus thrombosis produces venous infarction with hemorrhagic transformation and characteristic imaging findings of thrombosed sinuses, not isolated lobar microbleeds 1
Clinical Implications and Management Considerations
The diagnosis of CAA has critical therapeutic implications. 1, 6, 3
- Anticoagulation is contraindicated in patients with lobar microbleeds suggestive of CAA due to extremely high risk of catastrophic hemorrhage 6, 3
- Multiple microbleeds (≥4) predict future bleeding risk and absolutely contraindicate anticoagulation, even for atrial fibrillation 3
- The patient's current aspirin therapy should be carefully reconsidered given the hemorrhagic risk 6
- CAA-associated hemorrhages carry approximately 7% annual recurrence risk 6
Common Pitfalls to Avoid
Do not assume all microbleeds represent the same pathology. The topographic distribution is essential: lobar = CAA; deep/infratentorial = hypertensive arteriopathy 2, 1, 4
Do not rely on blood pressure alone to distinguish etiologies. This patient has only mild hypertension, and the lobar distribution of microbleeds overrides blood pressure considerations in determining etiology 2, 5
Do not miss the dementia connection. CAA is strongly associated with cognitive impairment through both hemorrhagic injury and shared amyloid pathology with Alzheimer's disease 5, 7