Posterior reversible encephalopathy syndrome with subarachnoid hemorrhage
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 hemorrhages. TOF-MIP is unremarkable without any higher grade proximal stenosis or aneurysm.
Vasogenic edema in the fronto-parietal and occipital lobes bilaterally. Subarachnoidal hemorrhage bifrontal and a few focal subcortical hemorrhages of the left frontal and occipital lobe. No hydrocephalus.
Case Discussion
Bilateral symmetrical vasogenic edema 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 hemorrhage in PRES is unclear. Doss-Esper et al have proposed 2 hypotheses: 1) nonaneurysmal subarachnoid (sulcal) hemorrhage 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 hemorrhages.