PRES and cerebral amyloid angiopathy

Case contributed by Dr Ian Bickle

Presentation

Elderly female with long standing hypertension. Altered sensorium. BP 224/104 mmHg.

Patient Data

Age: 82
Gender: Female
Modality: CT

Extensive bilateral periventricular deep white and subcortical white matter low attenuation, with a slight posterior predominance.

The sulci are poorly delineated for a patient of this age, suggesting a degree of oedema.

Bilateral basal ganglia calcification.

Modality: MRI

Extensive bilateral symmetrical periventricular deep white and subcortical high T2 signal change, with a slight posterior predominance.

Immumerable foci of SWI susceptability artifact through both cerebral and cerebellar hemispheres with sparing of the basal ganglia, thalami and brainstem.

Bilateral basal ganglia calcification.

No flow limiting arterial stenosis.

Case Discussion

PRES is a neurotoxic state that occurs due to difficulties in the cerebral circulations ability to autoregulate in response to acute changes in blood pressure. Hyperperfusion with resultant disruption of the blood brain barrier causes vasogenic oedema.  It is most commonly observed in the parieto-occipital regions ( hence the use of the name PRES) although as in this case it is not exclusive to the regions of the brain supplied by the posterior circulation.  It is typically symmetrical as in this case.

The widespread distribution of foci SWI susceptibility in this case with basal ganglia, thalami and brainstem sparing is more consistent with cerebral amyloid angiopathy.  This is opposed to chronic hypertensive angiopathy which has a predonderance for the basal ganglia and thalami.  The SWI appearances are similar representing 'micro-bleeds', but the distribution is different between cerebral amyloid and chronic hypertensive angiopathy.

 

 

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Case Information

rID: 48037
Case created: 15th Sep 2016
Last edited: 8th Jan 2017
Inclusion in quiz mode: Included

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