Presentation
Gastric outlet obstruction due to tumor. Pain crisis and profound hypertension (systolic > 200) resulting in status epilepticus and ICU admission.
Patient Data
There are focal regions of hypodensity and vasogenic edema involving the cortical and subcortical regions of the bilateral parietal and occipital lobes as well the bilateral cerebellum. There are also some focal hypodense regions within the bilateral frontal lobes, left more so than the right. This is associated with local overlying sulcal effacement. No intracranial hemorrhage.
Patchy bilateral but slightly asymmetric white matter T2/FLAIR hyperintensity are demonstrated in bilateral frontal lobes, parietal occipital lobes, cerebellar hemispheres, left corona radiata and in the left pons. There is a predominance in the parietal occipital lobes and the cerebellar hemispheres. There are some areas that demonstrate cortical involvement and gyral expansion. Multiple punctate foci of susceptibility artefact, in keeping with microhemorrhages, are demonstrated with a similar distribution, most prominent in the left frontal lobe. Punctate abnormal diffusion restriction, compatible with tiny infarcts, are seen in the right cerebellum, right parietal and bilateral frontal cortices. No definite subarachnoid hemorrhage. No abnormal enhancement. No hydrocephalus. No intracranial mass or collection. There is no convincing intracranial arterial irregularity on the time-of-flight MR angiogram allowing for artefact.
Conclusion: Findings are most in keeping with posterior reversible encephalopathy syndrome (PRES).
Case Discussion
Hypertension was treated and made an uneventful recovery. Most imaging changes resolved.
It is important to note that although PRES is thought of (and named) as a posterior/occipital process, it frequently involves other parts of the brain, including the cerebellum (~30-50% of the time) and deep grey matter and brainstem.
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