Cerebral amyloid angiopathy is amyloid-beta deposition in the walls of small brain vessels, and it is a common cause of lobar intracerebral haemorrhage (bleeding into the outer parts of the cerebral lobes) in older adults. After a first lobar haemorrhage, the question is what happens next. Recurrence, survival, and cognition each carry their own numbers.
Rebleeding is common and front-loaded. About one quarter of survivors experience a recurrent haemorrhage (pooled 23%, 95% CI 18-28%; the confidence interval is the range within which the true pooled figure plausibly lies). Risk rises with a prior haemorrhage, convexity subarachnoid blood (blood over the brain surface), cortical superficial siderosis (iron-containing blood residue along the brain surface, especially when disseminated), severe perivascular spaces in the centrum semiovale (enlarged fluid spaces around vessels in the deep white matter), and a larger index bleed (the first haemorrhage that brought the patient to attention).
Roughly half of survivors reach a favourable functional outcome at around a year and a half, while about one fifth to one quarter die. Poor outcome tracks with a lower admission consciousness level, recurrent bleeding, severe white-matter disease, and marked brain atrophy. These figures come from a single-centre cohort, so they guide counselling rather than individual prediction.
Dementia is the third trajectory. Among patients without early dementia after a lobar bleed, about one quarter develop dementia within a median of 2.5 years. Conversion is more likely with pre-existing mild cognitive impairment, heavy burden of white-matter hyperintensities (bright areas of white matter change on FLAIR MRI), disseminated siderosis, and a higher total small-vessel score (a combined MRI count of small-vessel disease markers). Cognitive decline also occurs in amyloid angiopathy without any haemorrhage, so dementia is not purely a post-bleed event.
Counselling has a unifying frame. Amyloid angiopathy and hypertensive arteriolosclerosis (hardening and thickening of small deep arteries from high blood pressure) together account for the great majority of spontaneous brain haemorrhages. Both create vessels in which antithrombotic drugs raise bleeding risk. Recurrence numbers and a medication review therefore belong in the same conversation. No primary-prevention strategy beyond vascular risk-factor control, principally blood pressure, has evidence behind it.