Posterior reversible encephalopathy syndrome with subarachnoid haemorrhage
Presentation
Sudden onset headache bifrontal, visual disturbance and apraxia. Severe hypertension. NIHHS 2, mRS 3. Obesity, tobacco use. No therapeutic anticoagulation.
Patient Data
T1 hypointense, T2 and FLAIR hyperintense subcortical signal changes in the fronto-parietal and the occipital lobes bilaterally without restricted diffusion. Small lesion of the posterior crus of internal capsule with bright signal in DWI and ADC (shine through effect) and some FLAIR-hyperintense lesions on both sides of the basal ganglia. A few tiny cortical and subcortical Foci of restricted diffusion fronto-parietal bilaterally. Sulcal FLAIR-hyperintensities in subarachnoidal space bifrontal and few focal subcortical areas of the hypointensities in gradient echo sequence of the left frontal lobe and the left occipital lobe consistent with sulcal subarachnoid and focal subcortical haemorrhages. TOF-MIP is unremarkable without any higher grade proximal stenosis or aneurysm.
Vasogenic oedema in the fronto-parietal and occipital lobes bilaterally. Subarachnoidal haemorrhage bifrontal and a few focal subcortical haemorrhages of the left frontal and occipital lobe. No hydrocephalus.
Case Discussion
Bilateral symmetrical vasogenic oedema pattern with severe hypertension in clinical history is classic for the posterior reversible encephalopathy syndrome (PRES).
The mechanism behind the coexistence of the sulcal subarachnoid haemorrhage in PRES is unclear. Doss-Esper et al have proposed 2 hypotheses: 1) nonaneurysmal subarachnoid (sulcal) haemorrhage due to rupture of pial vessels in the face of severe hypertension and impaired cerebral autoregulation, and 2) postischemic reperfusion injury leading to multifocal brain haemorrhages.