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Posterior reversible encephalopathy syndrome (PRES) represents a unique clinical entity with non-specific clinical symptoms and unique neuroradiological findings. This syndrome may present with a broad range of clinical symptoms from headache and visual disturbances to seizure and altered mentation. Typical imaging findings include posterior-circulation predominant vasogenic edema. Although there are many well-documented diseases associated with PRES, the exact pathophysiologic mechanism has yet to be fully elucidated. Generally accepted theories revolve around disruption of the blood-brain barrier secondary to elevated intracranial pressures or endothelial injury. In this article, we will review the clinical, typical, and atypical radiological features of PRES, as well as the most common theories behind the pathophysiology of PRES. Additionally, we will discuss some of the treatment strategies for PRES related to the underlying disease state.

Background: To explore blood–brain barrier disruption in hypertensive posterior reversible encephalopathy syndrome.Methods: The hypertension rat models were successfully established and scanned on 7T micro-MRI. MRI parameter maps including apparent diffusion coefficient, T1 value, and perfusion metrics such as cerebral blood volume, cerebral blood flow, mean transit time and time to peak maps, were calculated.Results: The ADC values of the experimental group were higher than those of the control group both in cortical (P < 0.01) and subcortical (P < 0.05) regions. Voxel-wise analysis of ADC maps localized vasogenic edema primarily to the posterior portion of the brain. The increase in cerebral blood volume and cerebral blood flow values were found in the cortical and subcortical regions of rats with acute hypertension. No correlation was found between perfusion metrics and mean arterial pressure. The Evans blue dye content was higher in the posterior brain region than the anterior one (P < 0.05).Conclusions: Cerebral vasogenic edema resulting from acute hypertension supports the hypothesis of posterior reversible encephalopathy syndrome as the result of blood–brain barrier disruption, which maybe the potential therapeutic target for intervention.

Objective: Diffusion-weighted imaging (DWI)-Alberta Stroke Program Early CT Score (ASPECTS) is a simple, widely used method to estimate the size of the infarct. Our aim is to determine whether there is a relationship between DWI-ASPECTS and fluid-attenuated inversion recovery (FLAIR) vascular hyperintensity (FVH)-DWI mismatch and to better quantify FVH-DWI mismatch to assess the prognosis of cerebral infarction.Materials and Methods: A retrospective analysis of 109 patients with MCA stenosis or occlusion with cerebral infarction was performed by dividing this cohort into FVH-DWI match group and FVH-DWI mismatch group based on FVH and DWI results. The clinical and imaging data of these two groups of patients were reviewed and analyzed to identify associations between FVH-DWI mismatch and prognosis of patients for preservation of neurological function. Correlation between DWI-ASPECTS and FVH-DWI mismatch was also performed.Results: FVH-DWI mismatch was present in 66/109 (60.55%) patients, and FVH-DWI match was present in 43/109 (39.45%). Patients with FVH-DWI mismatch had higher DWI-ASPECTS (7.0 vs. 4.0, P < 0.001) and lower mRS at 3 months (3.0 vs. 4.0, P < 0.001) than patients without FVH-DWI mismatch. Multiple regression analysis suggested that DWI-ASPECTS (OR = 4.7, 95% CI = 2.5–9.2, P < 0.001) remained significantly associated with FVH-DWI mismatch. Two threshold points for DWI-ASPECTS of 3 and 8 can be used to distinguish whether there is a mismatch in FVH-DWI by smooth curve fitting.Conclusions: The DWI-ASPECTS score was an independent predictor of FVH-DWI mismatch. At DWI-ASPECTS ≤ 3, the FVH-DWI mismatch offers no prognostic value; whereas, at DWI-ASPECTS ≥ 8, the FVH-DWI mismatch had the highest prognostic value. DWI-ASPECTS can roughly determine whether there is a FVH-DWI mismatch in order to select optimal clinical treatment and accurately assess prognosis.

In 2016, World Health Organization announced Zika virus infection and its neurological sequalae are a public health emergency of global scope. Preliminary studies have confirmed a relationship between Zika virus infection and certain neurological disorders, including microcephaly and Guillain–Barre syndrome (GBS). The neuroimaging features of microcephaly secondary to Zika virus infection include calcifications at the junction of gray–white matter and subcortical white matter with associated cortical abnormalities, diminution of white matter, large ventricles with or without hydrocephalus, cortical malformations, hypoplasia of cerebellum and brainstem, and enlargement of cerebellomedullary cistern. Contrast enhancement of the cauda equine nerve roots is the typical neuroimaging finding of GBS associated with Zika virus. This review describes the nervous system disorders and associated imaging findings seen in Zika virus infection, with the aim to improve the understanding of this disease. Imaging plays a key role on accurate diagnosis and prognostic evaluation of this disease.