DISCUSSION
Figure 1 is afluid-attenuated, inversion recovery T2-weighted MRI of the brain that shows ahyperintense signal within the white matter tracts of the parietooccipital lobes posteriorly and bilaterally. Figure 2 is a diffusion-weighted MRI image that demonstrates a small area of increased signal intensity in the right occipital lobe. This is compatible with an early infarct. The findings in Figure 1 are consistent with posterior reversible encephalopathy syndrome (PRES). Figure 2 reveals a small infarct in the right occipital lobe.
PRES, also known as reversible posterior leukoencephalopathy syndrome, is a condition that can be caused by several etiologies, butimaging findings are usually characteristic. Patients often present with headaches, hypertension, seizures, visual disturbances, and altered mental status. Other symptoms can include vomiting, impaired memory, lethargy, or agitation. Common precipitants include acutely elevated blood pressure, renal decompensation, fluidretention, preeclampsia or eclampsia, and treatment with immunosuppressive orantirejection drugs. Other associated clinical entities include systemic lupuserythematosus, thrombotic thrombocytopenia purpura, and hemolytic-uremicsyndrome. The antirejection and chemotherapeutic agents frequently associated with PRES include cyclosporine, tacrolimus, cisplatin, interferon alpha, and intrathecal methotrexate.1 Epoetin has also been associated with PRES. Thepathophysiology of PRES appears to be related to disorders of cerebral autoregulation and endothelial dysfunction, with two proposed mechanisms. Onesuggests there is cerebral vasospasm resulting in ischemia and cytotoxic edema. The other suggests vasodilatation is the causative factor resulting invasogenic edema.2 The posterior aspect of the brain is considered to be at greatest risk of insult, as there is less sympathetic innervation, making this area less able to adjust for changes in BP.3
MRI findings suggestive of PRES include white matter edema predominantly in the occipital and parietal lobes. This finding is fairly symmetric. PRES does not affect the calcarine and paramedian aspects of the occipital lobe; this characteristic distinguishes PRES from an infarct in the posterior cerebral artery (PCA) territory.4 Other areas of the brain, however, may be affected, including the brain stem, cerebellum, basal ganglia, and frontal lobes. CT findings appear as bilateral, fairly symmetric, low-attenuation areas in the posterior parietal and occipital lobes. The differential diagnosis includes PCA territory infarct, demyelinating disease, venous thrombus, vasculitis, or encephalitis.5
Prompt diagnosis of PRES is very important because, as the name implies, it can be reversible. Treatment includes stabilizing the BP, discontinuing or lowering the dose of causative drugs, and treating the seizures. With treatment, most patients have complete neurologic recovery within 2 weeks and imaging findings similarly resolve.6 If the syndrome is not treated, thecondition can progress to ischemia, infarction, epilepsy, and even death. Pregnant patients must be counseled about the signs and symptoms of preeclampsia, eclampsia, and late postpartum encephalopathy. JAAPA
Julie Vajnar is the department editor for Diagnostic Imaging Review and practices in a radiology group at North Oaks Health System,Hammond, Louisiana. She has indicated no relationships to disclose relating to the content of this article.
DRUGS MENTIONED
Cisplatin (Platinol-AQ)
Cyclosporine (Gengraf, Neorel, Sandimmune)
Epoetin (Erythropoietin Human Glycoform alpha)
Interferon alfa (Intron A [alfa-2b], Roferon-A [alfa-2a])
Methotrexate (Rheumatrex, Trexall)
Tacrolimus (Prograf)
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