Hypertensive microangiopathy, also referred to as chronic hypertensive encephalopathy, results from the sustained effects of elevated systemic blood pressure on the brain, leading to lipohyalinosis and Charcot-Bouchard aneurysms that are in turn prone to rupture resulting in hypertensive intracerebral hemorrhages.
The terms hypertensive microangiopathy and chronic hypertensive encephalopathy are not used uniformly in the literature but should probably be considered distinct from chronic small vessel disease despite hypertension being an important risk factor for it also. The latter is dominated by white matter change (leukoaraiosis) but does not necessarily have microhemorrhages.
Additionally, chronic hypertensive encephalopathy should not be confused with acute hypertensive encephalopathy - better known as posterior reversible encephalopathy syndrome (PRES).
The key finding of hypertensive microangiopathy is the presence of microhemorrhages affecting the basal ganglia, pons and cerebellar hemispheres . 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 .
There are a number of conditions to be considered:
- microhemorrhages secondary to cerebral amyloid angiopathy 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