scholarly journals Central-Variant Posterior Reversible Encephalopathy Syndrome with Albuminocytologic Dissociation

2018 ◽  
Vol 10 (1) ◽  
pp. 29-33 ◽  
Author(s):  
Sang-Woo Lee ◽  
Seung-Jae Lee
Keyword(s):  
Blood Brain Barrier ◽  
Posterior Reversible Encephalopathy Syndrome ◽  
Vasogenic Edema ◽  
Brain Magnetic Resonance Imaging ◽  
Cerebral Hemispheres ◽  
Brain Barrier ◽  
Posterior Reversible Encephalopathy ◽  
Blood Brain ◽  
Normal White Blood Cell ◽  
Reversible Encephalopathy

Posterior reversible encephalopathy syndrome (PRES) is a disorder of reversible vasogenic brain edema which mainly involves the parieto-occipital lobes in various clinical settings. The main mechanism is known to be cerebral autoregulation failure and endothelial dysfunction leading to the disruption of the blood-brain barrier. We report the case of a 47-year-old woman with PRES which involved the brain stem and thalami, sparing the cerebral hemispheres. She was admitted to the emergency room because of acute-onset confusion. Her initial blood pressure was 270/220 mm Hg. Routine blood lab tests showed pleocytosis, hyperglycemia, and azotemia. Brain magnetic resonance imaging (MRI) showed a lesion of vasogenic edema involving nearly the whole area of pons, the left side of the midbrain, and the bilateral medial thalami. Cerebrospinal fluid (CSF) examination revealed an increased level of protein with normal white blood cell count. With conservative care, the patient markedly recovered 3 days after symptom onset, and a follow-up MRI confirmed complete resolution of the vasogenic edema. This case suggests that PRES can rarely involve the “central zone” only, sparing the cerebral hemispheres, which may be confused with other neurological diseases. Besides, the CSF albuminocytologic dissociation may suggest the disruption of the blood-brain barrier in patients with PRES.

scholarly journals Posterior Reversible Encephalopathy Syndrome as Presenting Form of Very Early Systemic Sclerosis

2015 ◽  
Vol 2015 ◽  
pp. 1-3
Author(s):  
María Isabel Pedraza ◽  
Julia Barbado ◽  
Marina Ruiz ◽  
Ángel Luis Guerrero
Keyword(s):  
Systemic Sclerosis ◽  
Arterial Hypertension ◽  
Blood Brain Barrier ◽  
Posterior Reversible Encephalopathy Syndrome ◽  
Vascular Endothelium ◽  
Brain Barrier ◽  
Posterior Reversible Encephalopathy ◽  
Blood Brain ◽  
Reversible Encephalopathy ◽  
Early Systemic Sclerosis

Introduction. Posterior Reversible Encephalopathy Syndrome (PRES) is an increasingly recognized clinical and radiological entity with a wide spectrum of symptoms. Its mechanism depends on failure of the blood-brain barrier due to high systemic blood pressure (BP) and loss of integrity of vascular endothelium related with different triggers.Methods. We aim to report a case of PRES induced by arterial hypertension and very early systemic sclerosis (SSc) not previously known.Results. A 64-year-old female was admitted due to 1-week pulsating headache more prominent on frontal scalp, accompanied by phonophobia, photophobia, and facial flushing. Neurological exam revealed brisk deep tendon reflex. Brain magnetic resonance imaging (MRI) showed subcortical lesions mainly located in posterior regions. BP was monitored and episodic arterial hypertension was detected. In laboratory tests positive anti-topoisomerase I antibodies were detected. BP was controlled with angiotensin-converting-enzyme inhibitors and headache improved. In a new MRI a month later improvement of white matter lesions was observed. Capillaroscopy showed “active pattern,” considered typical of SSc.Conclusion. In SSc anti-endothelial cell antibodies impair vascular endothelium and liberation of vasoconstrictors leads to BP increasing and disruption of blood-brain barrier autoregulation mechanisms. PRES can be the first manifestation of very early SSc and this entity should be considered even in absence of skin lesions or Raynaud phenomenon.

scholarly journals Recurrent Posterior Reversible Encephalopathy Syndrome Potentially Related to AIDS and End-Stage Renal Disease: A Case Report and Review of the Literature

2012 ◽  
Vol 2012 ◽  
pp. 1-3 ◽  
Author(s):  
Olivia Hui-Chiun Chang ◽  
Alexandra Stanculescu ◽  
Chi Dola ◽  
William Benjamin Rothwell
Keyword(s):  
Renal Disease ◽  
Blood Brain Barrier ◽  
Posterior Reversible Encephalopathy Syndrome ◽  
End Stage Renal Disease ◽  
Brain Barrier ◽  
Posterior Reversible Encephalopathy ◽  
Blood Brain ◽  
Stage Renal Disease ◽  
End Stage ◽  
Reversible Encephalopathy

Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiological syndrome that is characterized by clinical features including headache, altered mental status, cortical blindness, seizures, and other focal neurological signs as well as subcortical edema without infarction on neuroimaging. Under the umbrella of hypertensive encephalopathy, PRES is defined by reversible cerebral edema due to dysfunction of the cerebrovascular blood-brain barrier unit. The pathophysiology of PRES is thought to result from abnormalities in the transmembrane flow of intravascular fluid and proteins caused by two phenomena: one, cerebral autoregulatory failure and two, loss of integrity of the blood-brain barrier. PRES is not a common disease in patients with human immunodeficiency virus (HIV) and AIDS with only three previously reported cases. Both the HIV and end-stage renal disease appear to further compromise the blood brain barrier. Although uncommon, PRES recurrence has been described. To the best of our knowledge, this is the first report demonstrating recurrent PRES in a HIV patient on hemodialysis for end-stage renal disease.

scholarly journals Posterior reversible encephalopathy syndrome following appendicitis in a young child: A case report and review of the pediatric literature

2021 ◽  
Vol 9 ◽  
pp. 2050313X2110534
Author(s):  
Yaseen Rafee ◽  
Ruba Allabwani ◽  
Tala Haddadin ◽  
Ahmad Kaddurah
Keyword(s):  
Posterior Reversible Encephalopathy Syndrome ◽  
Vasogenic Edema ◽  
Clinical Manifestations ◽  
Brain Magnetic Resonance Imaging ◽  
Altered Mental Status ◽  
Visual Disturbance ◽  
Complicated Appendicitis ◽  
Posterior Reversible Encephalopathy ◽  
Severe Infections ◽  
Reversible Encephalopathy

Posterior reversible encephalopathy syndrome is an acute or subacute neurological disorder with variable clinical manifestations including encephalopathy, headache, seizures, visual disturbance, and focal neurologic deficits. Neuroimaging often shows frequently reversible vasogenic edema that predominantly involves the subcortical parieto-occipital lobes. Posterior reversible encephalopathy syndrome has been associated with hypertension and reported in patients with many conditions including eclampsia/pre-eclampsia and immunosuppressive therapy. Recently, posterior reversible encephalopathy syndrome is recognized to occur in association with severe infections such as complicated appendicitis. Here, we describe a case of 11-year-old male admitted for complicated appendicitis and severe sepsis. He developed seizures and had an altered mental status 10 days into his hospitalization with brain magnetic resonance imaging findings consistent with posterior reversible encephalopathy syndrome. We review the pediatric literature and discuss the pathogenesis of posterior reversible encephalopathy syndrome in association with an infection. We highlight the importance of recognizing this syndrome as a possible cause for acute neurological deterioration in children with severe infections.

Posterior Reversible Encepalopathy Syndrome in A Child With Post Streptococcal Glomerulonephritis- A Rare Case Report

Med Phoenix ◽  
2021 ◽  
Vol 6 (1) ◽  
pp. 50-52
Author(s):  
Sunita Ghimire ◽  
Shree Krishna Shrestha ◽  
Ram Chandra Bastola ◽  
Anita Dahal ◽  
Pragya Shakya
Keyword(s):  
Posterior Reversible Encephalopathy Syndrome ◽  
Vasogenic Edema ◽  
Female Child ◽  
Hypertensive Encephalopathy ◽  
Posterior Reversible Encephalopathy ◽  
Radiological Features ◽  
Rare Case Report ◽  
Post Streptococcal Glomerulonephritis ◽  
Reversible Encephalopathy ◽  
Timely Treatment

Posterior reversible encephalopathy syndrome is a condition occurring  in majority of case of  hypertensive encephalopathy mainly due to vasogenic  edema in parieto occipital region in neuroimaging. It is reversible if timely treatment is done .Here we are reporting a 11 year old female child with acute post streptococal glomerulonephrtitis leading to typical clinical and radiological features of posterior reversible encephalopathy syndrome

scholarly journals Early Appearance of Activated Matrix Metalloproteinase-9 after Focal Cerebral Ischemia in Mice: A Possible Role in Blood—Brain Barrier Dysfunction

1999 ◽  
Vol 19 (9) ◽  
pp. 1020-1028 ◽  
Author(s):  
Yvan Gasche ◽  
Miki Fujimura ◽  
Yuiko Morita-Fujimura ◽  
Jean-Christophe Copin ◽  
Makoto Kawase ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Blood Brain Barrier ◽  
Focal Cerebral Ischemia ◽  
Vasogenic Edema ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Brain Barrier ◽  
Critical Event ◽  
Secondary Brain Injury ◽  
Blood Brain ◽  
Bbb Permeability

During cerebral ischemia blood–brain barrier (BBB) disruption is a critical event leading to vasogenic edema and secondary brain injury. Gelatinases A and B are matrix metalloproteinases (MMP) able to open the BBB. The current study analyzes by zymography the early gelatinases expression and activation during permanent ischemia in mice (n = 15). ProMMP-9 expression was significantly ( P < 0.001) increased in ischemic regions compared with corresponding contralateral regions after 2 hours of ischemia (mean 694.7 arbitrary units [AU], SD ± 238.4 versus mean 107.6 AU, SD ± 15.6) and remained elevated until 24 hours (mean 745,7 AU, SD ± 157.4). Moreover, activated MMP-9 was observed 4 hours after the initiation of ischemia. At the same time as the appearance of activated MMP-9, we detected by the Evan's blue extravasation method a clear increase of BBB permeability, Tissue inhibitor of metalloproteinase-1 was not modified during permanent ischemia at any time. The ProMMP-2 was significantly ( P < 0.05) increased only after 24 hours of permanent ischemia (mean 213.2 AU, SD ± 60.6 versus mean 94.6 AU, SD ± 13.3), and no activated form was observed. The appearance of activated MMP-9 after 4 hours of ischemia in correlation with BBB permeability alterations suggests that MMP-9 may play an active role in early vasogenic edema development after stroke.

scholarly journals Cerebral Edema Formation After Stroke: Emphasis on Blood–Brain Barrier and the Lymphatic Drainage System of the Brain

2021 ◽  
Vol 15 ◽  
Author(s):  
Sichao Chen ◽  
Linqian Shao ◽  
Li Ma
Keyword(s):  
Blood Brain Barrier ◽  
Cerebral Edema ◽  
Lymphatic System ◽  
Vasogenic Edema ◽  
Lymphatic Vessels ◽  
Drainage System ◽  
Brain Barrier ◽  
Edema Formation ◽  
Blood Brain ◽  
The Brain

Brain edema is a severe stroke complication that is associated with prolonged hospitalization and poor outcomes. Swollen tissues in the brain compromise cerebral perfusion and may also result in transtentorial herniation. As a physical and biochemical barrier between the peripheral circulation and the central nervous system (CNS), the blood–brain barrier (BBB) plays a vital role in maintaining the stable microenvironment of the CNS. Under pathological conditions, such as ischemic stroke, the dysfunction of the BBB results in increased paracellular permeability, directly contributing to the extravasation of blood components into the brain and causing cerebral vasogenic edema. Recent studies have led to the discovery of the glymphatic system and meningeal lymphatic vessels, which provide a channel for cerebrospinal fluid (CSF) to enter the brain and drain to nearby lymph nodes and communicate with the peripheral immune system, modulating immune surveillance and brain responses. A deeper understanding of the function of the cerebral lymphatic system calls into question the known mechanisms of cerebral edema after stroke. In this review, we first discuss how BBB disruption after stroke can cause or contribute to cerebral edema from the perspective of molecular and cellular pathophysiology. Finally, we discuss how the cerebral lymphatic system participates in the formation of cerebral edema after stroke and summarize the pathophysiological process of cerebral edema formation after stroke from the two directions of the BBB and cerebral lymphatic system.

scholarly journals Transient increase of fractional anisotropy in reversible vasogenic edema

2016 ◽  
Vol 36 (10) ◽  
pp. 1731-1743 ◽  
Author(s):  
Shihoko Kimura-Ohba ◽  
Yi Yang ◽  
Jeffrey Thompson ◽  
Tomonori Kimura ◽  
Victor M Salayandia ◽  
...  
Keyword(s):  
Fractional Anisotropy ◽  
Acute Phase ◽  
Cyclosporine A ◽  
Posterior Reversible Encephalopathy Syndrome ◽  
Pathological Condition ◽  
Neurological Diseases ◽  
Vasogenic Edema ◽  
High Dose ◽  
Posterior Reversible Encephalopathy ◽  
Reversible Encephalopathy

Brain vasogenic edema, involving disruption of the blood-brain barrier, is a common pathological condition in several neurological diseases, with a heterogeneous prognosis. It is sometimes reversible, as in posterior reversible encephalopathy syndrome, but often irreversible and our current clinical tools are insufficient to reveal its reversibility. Here, we show that increased fractional anisotropy in magnetic resonance imaging is associated with the reversibility of vasogenic edema. Spontaneously, hypertensive rats-stroke prone demonstrated posterior reversible encephalopathy syndrome-like acute encephalopathy in response to high-dose cyclosporine A treatment; the deteriorating neurological symptoms and worsening scores in behavioral tests, which were seen in acute phase, dissappered after recovery by cessation of cyclosporine A. In the acute phase of encephalopathy, the fractional anisotropy and apparent diffusion coefficient increased in areas with IgG leakage. This increase of fractional anisotropy occurred in the absence of demyelination: fluid leakage into the myelinated space increased the axial, but not the radial, diffusivity, resulting in the increased fractional anisotropy. This increased fractional anisotropy returned to pre-encephalopathy values in the recovery phase. Our results highlight the importance of the fractional anisotropy increase as a marker for the reversibility of brain edema, which can delineate the brain areas for which recovery is possible.

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