SUMMARY: PRES is a clinicoradiologic entity, combining seizures, blindness, and coma with MR imaging findings of predominantly vasogenic and occasional cytotoxic edema. In this clinical report, we determined the type of edema by using DWI and FLAIR sequences on MR imaging as well as ADC maps in 28 patients with PRES. The neuradiologic findings were correlated with levels of serum albumin, which is a main contributor to colloid osmotic pressure and vascular integrity. The presence of vasogenic edema was significantly associated with decreased serum albumin levels, which may be a particular risk factor for the development of PRES.ABBREVIATIONS: ADC ϭ apparent diffusion coefficient; ANOVA ϭ analysis of variance; CI ϭ confidence interval; COP ϭ colloid osmotic pressure; DWI ϭ diffusion-weighted imaging; FLAIR ϭ fluid-attenuated inversion recovery; IL ϭ Interleukin; KS ϭ Kolmogorov-Smirnov; MWU ϭ Mann Whitney U; NO ϭ nitric oxide; PRES ϭ posterior reversible encephalopathy syndrome; ROS ϭ reactive oxygen species P RES is a clinicoradiologic entity with acute onset of seizures, blindness, alterations of consciousness, and headache. MR imaging is of great importance in the diagnosis of this clinically inhomogeneous syndrome, which typically shows bilateral signal-intensity alterations in cortical and subcortical regions of the posterior circulation, indicating vasogenic edema.1 A low proportion of patients show cytotoxic edema or lesions outside the posterior circulation.2 An association between the etiology of PRES and MR imaging findings has been negated in a recent investigation.3 Additionally, it remains unclear why patients develop either vasogenic or cytotoxic edema in PRES. Cytotoxic and vasogenic edema in PRES can be differentiated by using DWI and FLAIR sequences. 4 It has been postulated that PRES is caused by endothelial damage and dysfunctional cerebral autoregulation due to excessive hypertension, leading to hyperperfusion and subsequent vasogenic edema in susceptible vessels. 5,6 Other risk factors are pre-eclampsia, sepsis, cytotoxic and immunosuppressant drugs, and nephrotic syndrome.7 These conditions all involve high oxidative stress and a systemic proinflammatory process, 8 hinting at additional mechanisms involved in PRES pathogenesis, such as vasoactive substances, vasospasm, and microinfarctions. 9 As seen in nephrotic syndrome, most diseases associated with PRES exhibit significantly reduced serum albumin levels.10 Serum albumin accounts for 75% of plasma protein and, therefore, is a main contributor to COP, reducing perfusion pressure, which results in retention of fluid in the vessel.
11Vasogenic edema can be aggravated by a marked decrease in COP. 12 Albumin protects vascular endothelial cells from oxidative stress and damage, 13 acting as an important antioxidant that preserves vascular integrity.This clinical report describes 28 patients with PRES and focuses on the type of edema in correlation with serum albumin. We show that vasogenic edema in PRES occurs significantly more often in patien...