Hypertensive microangiopathy, also referred to as chronic hypertensive encephalopathy (not to be confused with acute hypertensive encephalopathy, better known as PRES) results from the sustained effects of elevated systemic blood pressure on the brain.
The key finding of hypertensive microangiopathy is the presence of microhemorrhages affecting the basal ganglia, pons and cerebellar hemispheres 1. This is, not surprisingly, the same distribution as macroscopic hypertensive intracerebral hemorrhages.
These are best seen on T2* sequences, particularly susceptibility weighted imaging (SWI) as small blooming areas of signal loss 1.
There are a number of conditions to be considered:
- microhemorrhages secondary to cerebral amyloid angiopathy (CAA)
- peripherally distributed, in the same distribution as lobar hemorrhages
- multiple cavernous malformations as seen in familial multiple cavernous malformation syndrome
- randomly distributed
- some are larger
- calcified/treated metastases
- usually larger
- more peripheral