Corticosteroids in posterior reversible encephalopathy syndrome:Friend or foe?A systematic review

BACKGROUND Posterior reversible encephalopathy syndrome(PRES)is a complex neurological disorder characterized by symptoms such as headaches,seizures,confusion,and visual disturbances.The pathophysiology of PRES involves endothelial dysfunction,disrupted cerebral autoregulation,and resulting vasogenic edema.Hypertension and other factors that alter cerebral autoregulation are critical in its development.Corticosteroids,widely used for their anti-inflammatory and immunosuppressive properties,play a controversial role in PRES.AIM To elucidate the dual role of corticosteroids in the context of PRES by critically evaluating the existing literature.Specifically,it seeks to assess the results of PRES induced by corticosteroid therapy and the efficacy and safety of corticosteroids in the treatment of PRES.By synthesizing case reports and series,this review aims to provide a comprehensive understanding of the mechanisms,clinical presentations,and management strategies associated with corticosteroid-related PRES.METHODS The review was carried out according to the PRISMA guidelines.The databases searched included Science Direct,PubMed,and Hinari.The search strategy encompassed terms related to corticosteroids and PRES.Studies were included if they were peer-reviewed articles examining corticosteroids in PRES,excluding non-English publications,reviews,and editorials.Data on patient demographics,clinical characteristics,imaging findings,corticosteroid regimens,and outcomes were extracted.The risk of bias was evaluated using the Joanna Briggs Institute tool for case reports.RESULTS A total of 56 cases of PRES(66.1%women,33.9%men)potentially induced by corticosteroids and 14 cases in which corticosteroids were used to treat PRES were identified.Cases of PRES reportedly caused by corticosteroids showed a mean age of approximately 25.2 years,with seizures,headaches,hypertension,and visual disturbances being common clinical sequelae.Magnetic resonance findings typically revealed vasogenic edema in the bilateral parieto-occipital lobes.High-dose or prolonged corticosteroid therapy was a significant risk factor.On the contrary,in the treatment cases,corticosteroids were associated with positive outcomes,including resolution of vasogenic edema and stabilization of symptoms,particularly in patients with underlying inflammatory or autoimmune diseases.CONCLUSION Corticosteroids have a dual role in PRES,capable of both inducing and treating the condition.The current body of literature suggests that corticosteroids may play a greater role as a precipitating agent of PRES rather than treating.Corticosteroids may induce PRES through hypertension and subsequent increased cerebral blood flow and loss of autoregulation.Corticosteroids may aid in the management of PRES:(1)Enhancing endothelial stability;(2)Antiinflammatory properties;and(3)Improving blood-brain barrier integrity.Mechanisms which may reduce or mitigate vasogenic edema formation.

The apparent diffusion coefficient does not reflect cytotoxic edema on the uninjured side after traumatic brain injury

After traumatic brain injury, vasogenic and cytotoxic edema appear sequentially on the involved side. Neuroimaging investigations of edema on the injured side have employed apparent diffusion coefficient measurements in diffusion tensor imaging. We investigated the changes occurring on the injured and uninjured sides using diffusion tensor imaging/apparent diffusion coefficient and histological samples in rats. We found that, on the injured side, that vasogenic edema appeared at 1 hour and intracellular edema appeared at 3 hours. Mixed edema was observed at 6 hours, worsening until 12–24 hours post-injury. Simultaneously, microglial cells proliferated at the trauma site. Apparent diffusion coefficient values increased at 1 hour, decreased at 6 hours, and increased at 12 hours. The uninjured side showed no significant pathological change at 1 hour after injury. Cytotoxic edema appeared at 3 hours, and vasogenic edema was visible at 6 hours. Cytotoxic edema persisted, but vasogenic edema tended to decrease after 12–24 hours. Despite this complex edema pattern on the uninjured side with associated pathologic changes, no significant change in apparent diffusion coefficient values was detected over the first 24 hours. Apparent diffusion coefficient values accurately detected the changes on the injured side, but did not detect the changes on the uninjured side, giving a false-negative result.

Posterior reversible encephalopathy syndrome due to seronegative systemic lupus erythematosus

Posterior reversible encephalopathy syndrome(PRES)is a neurotoxic state coupled with a unique computed tomography or magnetic resonance imaging(MRI)appearance.Recognized in the setting of a number of complex conditions(preeclampsia/eclampsia,allogeneic bone marrow transplantation,organ transplantation,autoimmune disease and high-dose chemotherapy)in the imaging,clinical and laboratory features of this toxic state are becoming better elucidated.We are presenting a case of PRES due to seronegative systemic lupus erythematosus,with MRI findings of diffuse vasogenic edema.

Early Neurological Deterioration after Recanalization Treatment in Patients with Acute Ischemic Stroke： A Retrospective Study

Background： Early neurological deterioration （END） is a prominent issue after recanalization treatment. However. few studies have reported the characteristics of END after endovascular treatment （EVT） as so far. This study investigated the incidence, composition, and outcomes of END after intravenous recombinant tissue plasminogen activator （IV rt-PA） and EVT of acute ischemic stroke, and identified risk factors for END. Methods： Medical records of patients who received recanalization treatment between January l, 2014, and December 31, 2015 were reviewed. Patients were classified into IV rt-PA or EVT group according to the methods ofrecanalization treatment. The END was defined as an increase in the National Institutes of Health Stroke Scale （N1HSS） ≥4 or an increase in la of NIHSS ≥I within 72 h after recanalization treatment. Clinical data were compared between the END and non-END subgroups within each recanalization group. Results： Of the 278 patients included in the study, the incidence of END was 34.2%. The incidence rates of END were 29.8% in the IV rt-PA group and 40.2% in the EVT group, lschemia progression （68.4%） was the main contributor to END followed by vasogenic cerebral edema （21. 1%） and symptomatic intracranial hemorrhage （10.5%）. Multivariate logistic regression showed that admission systolic blood pressure （SBP） ≥160 mmHg （odds ratio [OR]： 2.312, 95% confidence interval [CI]： 1.105-4.837） and large artery occlusion after IV rt-PA （OR： 3.628.95% （7： 1.482-8.881 ） independently predicted END after IV rt-PA; and admission SBP 〉 140 mmHg （OR： 5.183, 95% CI：1.967 13.661 ）, partial recanalization （OR： 4.791,95% CI： 1.749-13.121 ）, and nonrecanalization （OR： 5.952, 95% CI： 1.841-19.243） independently predicted END alter EVT. The mortality rate and grave outcome rate at discharge of all the END patients （26.3% and 55.8%） were higher than those of all the non-END patients （1.1% and 18.6%： P 〈 0.01）. Conclusions： END was not an uncommon event and associated with death and grave outcome at discharge. High admission SBP and unsatisfactory recanalization of occluded arteries might predict END.