Posterior Reversible Encephalopathy Syndrome (PRES) With Immune System Activation, VEGF Up-Regulation, and Cerebral Amyloid Angiopathy

Kofler, Julia; Bartynski, Walter S.; Reynolds, Thomas Q.; Lieberman, Frank S.; Murdoch, Geoffrey; Hamilton, Ronald L.

doi:10.1097/rct.0b013e3181f31917

Cited by 25 publications

(14 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Additional evidence from a brain biopsy included endothelial cell activation, T-cell trafficking, and increased expression of vascular endothelial growth factor, all indicating inflammation. 6 The authors concluded that PRES was triggered by inflammation from an upper respiratory infection the patient had earlier. In contrast, Bernstein and colleagues interpreted a similar finding as CAA-induced inflammation (CAA-I) and stated that the resolution of symptoms was due to successful steroid treatment.…”

Section: Discussionmentioning

confidence: 99%

“…However, MRI with gradient-echo sequences now allows detection of small cortical and subcortical hemorrhages and thus, diagnosis of different CAA phenotypes including hemosiderosis (SH), acute cerebral ischemia, and superficial and posterior reversible encephalopathic syndrome (PRES). For the diagnosis of the latter, diffusion-weighted imaging and fluid-attenuated inversion recovery imaging (FLAIR) 6–9 are required.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Amyloid-β Contributes to Blood–Brain Barrier Leakage in Transgenic Human Amyloid Precursor Protein Mice and in Humans With Cerebral Amyloid Angiopathy

Hartz

Bauer

Soldner

et al. 2012

Stroke

213

172

View full text Add to dashboard Cite

Background and Purpose Cerebral amyloid angiopathy (CAA) is a degenerative disorder characterized by amyloid-β (Aβ) deposition in the blood–brain barrier (BBB). CAA contributes to injuries of the neurovasculature including lobar hemorrhages, cortical microbleeds, ischemia, and superficial hemosiderosis. We postulate that CAA pathology is partially due to Aβ compromising the BBB. Methods We characterized 19 patients with acute stroke with “probable CAA” for neurovascular pathology based on MRI and clinical findings. Also, we studied the effect of Aβ on the expression of tight junction proteins and matrix metalloproteases (MMPs) in isolated rat brain microvessels. Results Two of 19 patients with CAA had asymptomatic BBB leakage and posterior reversible encephalopathic syndrome indicating increased BBB permeability. In addition to white matter changes, diffusion abnormality suggesting lacunar ischemia was found in 4 of 19 patients with CAA; superficial hemosiderosis was observed in 7 of 9 patients. Aβ40 decreased expression of the tight junction proteins claudin-1 and claudin-5 and increased expression of MMP-2 and MMP-9. Analysis of brain microvessels from transgenic mice overexpressing human amyloid precursor protein revealed the same expression pattern for tight junction and MMP proteins. Consistent with reduced tight junction and increased MMP expression and activity, permeability was increased in brain microvessels from human amyloid precursor protein mice compared with microvessels from wild-type controls. Conclusions Our findings indicate that Aβ contributes to changes in brain microvessel tight junction and MMP expression, which compromises BBB integrity. We conclude that Aβ causes BBB leakage and that assessing BBB permeability could potentially help characterize CAA progression and be a surrogate marker for treatment response.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Amyloid-β Contributes to Blood–Brain Barrier Leakage in Transgenic Human Amyloid Precursor Protein Mice and in Humans With Cerebral Amyloid Angiopathy

Hartz

Bauer

Soldner

et al. 2012

Stroke

213

172

View full text Add to dashboard Cite

show abstract

“…[9, 10] Endothelial dysfunction leading to vasoconstriction is thought to occur as a result of an underlying milieu of immune activation with elicitation of vasoactive factors that have a deleterious effect on the cerebral endothelium. [6, 11] Some form of immuno-modulation is common to most, if not all, PRES-predisposing conditions. [6] Additionally, in the rare reported biopsy/autopsy cases of PRES, immune activation as manifested by endothelial activation, T-cell trafficking, and vascular endothelial growth factor expression (VEGF) has been observed.…”

Section: Discussionmentioning

confidence: 99%

“…[6] Additionally, in the rare reported biopsy/autopsy cases of PRES, immune activation as manifested by endothelial activation, T-cell trafficking, and vascular endothelial growth factor expression (VEGF) has been observed. [11, 12] Thus, PRES is increasingly viewed as a state of hypoperfusion that occurs as a result of immune activation/dysfunction eventually leading to vasoconstriction within the cerebral arterial vasculature.…”

Section: Discussionmentioning

confidence: 99%

Features of infratentorial-predominant posterior reversible encephalopathy syndrome

et al. 2015

View full text Add to dashboard Cite

Introduction PRES is a neurotoxic process that typically occurs in the setting of immune dysregulation. In contrast to the characteristic pattern involving parieto-occipital and posterior frontal regions, predominant involvement of the infratentorial brain occurs in a minority of PRES patients. We examined six patients with IPPRES relative to those with typical PRES in terms of clinical factors of toxicity and outcomes. We review the current understanding of PRES pathophysiology. Methods An institutional database of PRES patients was created through an IRB-approved search of the electronic record from 2007-2012. MR images were reviewed and classified by two neuroradiologists. Clinical data including laboratory data, blood pressure, and discharge outcome were collected through review of existing electronic medical records. Characteristics of the two groups were compared. Results Six cases among 80 PRES patients displayed an atypical distribution of signal abnormality predominantly involving the infratentorial brain. In IPPRES patients, signal abnormalities within the supratentorial brain, when present, showed a predominantly central distribution rather than the typical peripheral distribution. IPPRES patients showed higher rates of extreme hypertension, renal dysfunction, abnormal serum calcium, and abnormal serum magnesium relative to typical PRES patients. Outcomes were similar between the two groups. Discussion In our small series, IPPRES differs from typical PRES patients not only in the distribution of imaging abnormalities but also in rates of extreme hypertension and several laboratory indices. Despite these differences, clinical outcome in the IPPRES group was similar to that of typical PRES.

show abstract

“…However, watershed hypoperfusion and reduced brain perfusion in the posterior brain region have also been proposed by previous studies (13,14). At present, the intrinsic mechanism of RPES is considered to be an evolving systemic process with hypoperfusion/vasoconstriction and the development of brain toxicity, involving immune system activation, endothelial cell injury and inflammatory cytokine responses (15,16). The aforementioned toxicity-associated hypoperfusion/vasoconstriction leads to capillary bed injury and vasogenic edema.…”

Section: A B C Dmentioning

confidence: 99%

Reversible posterior encephalopathy syndrome associated with late onset postpartum eclampsia: A case report

Yang

Wang

2016

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

Abstract. Late onset postpartum eclampsia (LPE) is defined by its onset at >48 h after delivery. Reversible posterior encephalopathy syndrome (RPES) associated with LPE is uncommon, with the majority of RPES cases having a late postpartum onset within 4 weeks after childbirth. The present study reported the case of a 15-year old female presenting with convulsions that began 5 weeks after delivery. A magnetic resonance imaging scan of the brain revealed multiple lesions in the cortex, subcortical region and deep white matter of the bilateral cerebellum, and occipital, frontal and parietal lobes. The clinical manifestations and radiological abnormalities were readily resolved subsequent to antihypertension and anticonvulsion treatment. In conclusion, the present rare case indicates that LPE should be considered as a potential diagnosis even at 4 weeks after delivery. Furthermore, clinicians should familiarize with the reversible radioimaging features of RPES, since early recognition and adequate treatment are important to the outcome of patients.

show abstract

Posterior Reversible Encephalopathy Syndrome (PRES) With Immune System Activation, VEGF Up-Regulation, and Cerebral Amyloid Angiopathy

Cited by 25 publications

References 18 publications

Amyloid-β Contributes to Blood–Brain Barrier Leakage in Transgenic Human Amyloid Precursor Protein Mice and in Humans With Cerebral Amyloid Angiopathy

Amyloid-β Contributes to Blood–Brain Barrier Leakage in Transgenic Human Amyloid Precursor Protein Mice and in Humans With Cerebral Amyloid Angiopathy

Features of infratentorial-predominant posterior reversible encephalopathy syndrome

Reversible posterior encephalopathy syndrome associated with late onset postpartum eclampsia: A case report

Contact Info

Product

Resources

About