Posterior reversible encephalopathy syndrome (PRES)

Findings

Diffuse hyperintensity is present in the cortical and subcortical parietal, occipital, and frontal white matter (all figures). No diffusion restriction is present on the DWI (images not shown). The ADC signal is increased (images not shown). Hypodensity is seen in the corresponding areas on the CT of the brain. These findings are most compatible with PRES.

Differential diagnosis:
- Posterior reversible encephalopathy syndrome (PRES)
- Acute PCA infarction
- Hypotensive stroke
- Severe hypoglycemia
- Progressive multifocal leukoencephalopathy
- Gliomatosis cerebri


Diagnosis: Posterior reversible encephalopathy syndrome (PRES)


PRES has been associated with several conditions, such as acute glomerulonephritis, thrombotic thrombocytopenic purpurpa, and hemolytic uremic syndrome, drug toxicity, cryoglobinemia, and systemic lupus erythematosis. Drug toxicity from Cisplatin, interferon, erythropoietin, tacrolimus, and cyclosporin has been documented as a cause of PRES. Most cases are thought to be the result of inability of the posterior circulation to autoregulate blood flow in the setting of acute hypertension. This in turn leads to endothelial and blood brain barrier injury with resultant vasogenic edema. Patients typically have signs or symptoms of headache, mental status changes, acute hypertension, and seizures. When imaging findings are compatible with PRES, one should also search for potential complications, including hemorrhage and stroke. Follow-up imaging should be performed when the hypertension is reversed. Most patients respond well with hypertensive management and treatment of the underlying etiology.

Cranial computed tomographic images frequently show low attenuating cortical or subcortical lesions, primarily in the posterior parietal and occipital lobes. Hypodense foci may be seen in the frontal and temporal lobes. Additional symmetric lesions may occur in the basal ganglia and brainstem with less frequency. MR will show hypointense lesions on T1-weighted imaging with corresponding hyperintensity on the T2-weighted imaging - FLAIR images. ADC images will have increased diffusion coefficients secondary to vasogenic edema. Diffusion-weighted imaging is usually normal. If diffusion restriction is present with decreased ADC values, cytotoxic edema may be present. With contrast, patchy enhancement may be seen. Diffusion tensor imaging shows increased brain water diffusion.