Posterior reversible encephalopathy syndrome (PRES) is characterized by vasogenic edema, usually reversible, with the prominent involvement of the parietal and occipital lobes. The exact etiopathogenesis leading to PRES is unknown. Because signs of eclampsia and preeclampsia in neuroimaging often overlap and manifest as PRES, we aimed to evaluate whether demographic, clinical, and laboratory parameters predict PRES in patients with preeclampsia or eclampsia.

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213 pre-eclampsia or eclampsia patients with cranial imaging were retrospectively examined. We recorded the patients’ demographic information, systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), hemogram, biochemical indicators, clinical symptoms, and imaging features.

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Of all patients, 69% (n = 147) had preeclampsia while 31% (n = 66) had eclampsia, and 24.4% (n = 53) were diagnosed with PRES. The mean age of patients who developed PRES was 25.81 ± 6.07 years and thus significantly less than that of patients who did not develop PRES (p = .000). Patients with PRES had significantly higher mean SBP (p = .015), DBP (p = .009), and MAP (p = .003) than patients without PRES, along with significantly higher aspartate aminotransferase (ASAT; p = .001), alanine aminotransferase (ALAT; p = .001) blood urea nitrogen (BUN; p = .001), white blood cell (WBC; p = .003), neutrophil (p = .001), and hemoglobin (Hb; p = .027) levels, but significantly lower albumin (p = .000) levels.

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Age, high blood pressure, and BUN, neutrophil, and WBC levels were predictors of the development of PRES in patients with preeclampsia and eclampsia. Early neuroimaging considering those predictors should be performed to diagnose PRES in patients with preeclampsia and eclampsia.

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A posterior reverzibilis encephalopathia szindrómát (PRES) általában reverzibilis vasogen oedema jellemzi, ami leginkább a parietalis és occipitalis lebenyeket érinti. A PRES kialakulásához vezető pontos etiopatogenezis ismeretlen. Mivel az eclampsia és a praeeclampsia jelei az idegi képalkotó vizsgálatokon gyakran átfedik egymást, és PRES-ként manifesztálódnak, célunk annak értékelése volt, hogy a praeeclampsiás vagy eclampsiás betegeknél a demográfiai, klinikai és laboratóriumi paraméterek előre jelzik-e a PRES-t.

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213 olyan preeclampsiás vagy eclampsiás beteget vontunk be retrospektív módon, akiknél koponyaűri képalkotó vizsgálatot végeztek. Feljegyeztük a betegek demográfiai adatait, szisztolés vérnyomását (SBP), diasztolés vérnyomását (DBP), átlagos artériás nyomását (MAP), hemogramját, biokémiai mutatóit, klinikai tüneteit és képalkotó jellemzőit.

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A betegek 69%-ánál (n = 147) praeeclampsiát, 31%-ánál (n = 66) eclampsiát, 24,4%-ánál (n = 53) pedig PRES-t diagnosztizáltak. Azok a betegek, akiknél PRES alakult ki, szignifikánsan alacsonyabb átlagéletkorral (25,81 ± 6,07 év) bírtak, mint azok, akiknél nem alakult ki PRES (p = 0,000). A PRES-ben szenvedő betegeknél szignifikánsan magasabb volt az átlagos SBP (p = 0,015), a DBP (p = 0,009) és a MAP (p = 0,003), mint a PRES nélküli betegeknél, valamint szignifikánsan magasabb volt a következők vérszintje: glutamát-oxálacetát-transzamináz (aszpartát-aminotranszferáz/ASAT; p = 0,001), glutamát-piruvát-transzamináz (alanin-aminotransz-feráz/ALAT; p = 0,001), karbamid-nitrogén (BUN; p = 0,001), fehérvérsejtszám (WBC; p = 0,003), neutrophilsejt-szám (p = 0,001) és hemoglobin (Hb; p = 0,027), míg szignifikánsan alacsonyabb az albumin- (p = 0,000) szint.

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Az életkor, a magas vérnyomás, valamint a BUN-, a neutrophilsejt- és a WBC-szintek a praeeclampsiás és eclampsiás betegeknél a PRES kialakulásának előrejelzői voltak. Ezeket a prediktív tényezőket figyelembe véve a praeeclampsiás és eclampsiás betegeknél a PRES diagnosztizálásának érdekében korán érdemes idegi képalkotó vizsgálatot végezni.

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BACKGROUND: Guillain-Barré syndrome (GBS) is an autoimmune disorder characterized by demyelination of peripheral nerves. GBS-associated posterior reversible encephalopathy syndrome (PRES) is a rare and potentially life-threatening complication in the pediatric population. We aimed to report and analyze the clinical features, management, and outcomes of three cases of GBS-associated PRES in our setting in the light of the existing literature.
METHODS: Medical records of 75 pediatric patients with GBS were reviewed for autonomic changes and GBS-associated PRES. Thirty-one developed dysautonomia while three were identified to have PRES. Clinical, radiological, laboratory, and treatment data were collected and analyzed.
RESULTS: All three patients were male and presented with symptoms of acute flaccid paralysis and respiratory distress requiring mechanical ventilation. All three patients experienced various complications, including hypertension, seizures, and hyponatremia, and were subsequently diagnosed with PRES. Multimodal intensive care resulted in patient improvement and discharge in an ambulatory state after an average of 104 days of care.
CONCLUSIONS: GBS-associated PRES is a rare and potentially life-threatening complication that can occur in pediatric patients with GBS. Our findings suggest that early recognition, prompt intervention, and multimodal intensive care can improve patient outcomes. Further studies are needed to determine optimal treatment strategies for GBS-associated PRES.

Posterior reversible encephalopathy syndrome (PRES) is an acute neurological condition associated with different etiologies, including antibiotic therapy. To date, most data regarding antibiotic-related PRES are limited to case reports and small case series. Here, we report a novel case description and provide a systematic review of the clinico-radiological characteristics and prognosis of available cases of PRES associated with antibiotic therapy. We performed a systematic literature search in PubMed and Scopus from inception to 10 January 2024, following PRISMA guidelines and a predefined protocol. The database search yielded 12 subjects (including our case). We described the case of a 55-year-old female patient with PRES occurring one day after administration of metronidazole and showing elevated serum neurofilament light chain protein levels and favorable outcome. In our systematic review, antibiotic-associated PRES was more frequent in female patients (83.3%). Metronidazole and fluoroquinolones were the most reported antibiotics (33.3% each). Clinical and radiological features were comparable to those of PRES due to other causes. Regarding the prognosis, about one third of the cases were admitted to the intensive care unit, but almost all subjects (90.0%) had a complete or almost complete clinical and radiological recovery after prompt cessation of the causative drug. Antibiotic-associated PRES appears to share most of the characteristics of classic PRES. Given the overall good prognosis of the disease, it is important to promptly diagnose antibiotic-associated PRES and discontinue the causative drug.

BACKGROUND: Posterior reversible encephalopathy syndrome (PRES) and reversible cerebral vasoconstriction syndrome (RCVS) may cause ischaemic stroke and intracranial haemorrhage. The aim of our study was to assess the frequency of the afore-mentioned outcomes.
METHODS: We performed a PROSPERO-registered (CRD42022355704) systematic review and meta-analysis accessing PubMed until 7 November 2022. The inclusion criteria were: (1) original publication, (2) adult patients (≥18 years), (3) enrolling patients with PRES and/or RCVS, (4) English language and (5) outcome information. Outcomes were frequency of (1) ischaemic stroke and (2) intracranial haemorrhage, divided into subarachnoid haemorrhage (SAH) and intraparenchymal haemorrhage (IPH). The Cochrane Risk of Bias tool was used.
RESULTS: We identified 848 studies and included 48 relevant studies after reviewing titles, abstracts and full text. We found 11 studies on RCVS (unselected patients), reporting on 2746 patients. Among the patients analysed, 15.9% (95% CI 9.6%-23.4%) had ischaemic stroke and 22.1% (95% CI 10%-39.6%) had intracranial haemorrhage. A further 20.3% (95% CI 11.2%-31.2%) had SAH and 6.7% (95% CI 3.6%-10.7%) had IPH. Furthermore, we found 28 studies on PRES (unselected patients), reporting on 1385 patients. Among the patients analysed, 11.2% (95% CI 7.9%-15%) had ischaemic stroke and 16.1% (95% CI 12.3%-20.3%) had intracranial haemorrhage. Further, 7% (95% CI 4.7%-9.9%) had SAH and 9.7% (95% CI 5.4%-15%) had IPH.
CONCLUSIONS: Intracranial haemorrhage and ischaemic stroke are common outcomes in PRES and RCVS. The frequency reported in the individual studies varied considerably.

We systematically reviewed case reports of posterior reversible encephalopathy syndrome (PRES), and investigated the characteristics of PRES in pregnant Japanese women and the clinical relevance of reversible cerebral vasoconstriction syndrome (RCVS) in pregnant women with PRES. Articles were collected using the PubMed/Medline and Ichushi-Web databases. This review was ultimately conducted on 121 articles (162 patients). The clinical characteristics of PRES, individual sites of PRES lesions, edema types, and clinical characteristics of RCVS in PRES cases were examined. The most common individual site of PRES lesion was the occipital lobe (83.3%), followed by the basal ganglia, parietal lobe, frontal lobe, brain stem, cerebellum, temporal lobe, thalamus, and splenium corpus callosum (47.5, 42.6, 24.7, 16.1, 9.3, 5.6, 4.3, and 0.0%, respectively). Edema types in 79 cases with PRES were mainly the vasogenic edema type (91.1%), with very few cases of the cytotoxic edema type (3.8%) and mixed type (5.1%). Among 25 PRES cases with RCVS, RCVS was not strongly suspected in 17 (68.0%) before magnetic resonance angiography. RCVS was observed at the same time as PRES in 13 cases (approximately 50%), and between days 1 and 14 after the onset of PRES in the other 12. These results suggest that the basal ganglia is a frequent site of PRES lesions in pregnant women. RCVS may occur at or after the onset of PRES, even if there are no symptoms to suggest RCVS.

Tacrolimus, a calcineurin inhibitor, is an immunosuppressant used globally to prevent rejection after organ transplantation. Although it significantly improves outcomes for solid organ transplant patients, it is associated with various side effects such as nephrotoxicity and neurotoxicity. Tacrolimus-induced neurotoxicity is frequently encountered in clinical practice and can present with a variety of symptoms that may occur even at therapeutic levels. Although tacrolimus-induced neurotoxicity is well documented, there is limited literature available on pharmacologic management. Twenty-eight case reports of tacrolimus-induced neurotoxicity were identified and analyzed in addition to other literature including reviews, retrospective studies, and animal model studies. The severity of cases of tacrolimus-induced neurotoxicity reported ranged from mild symptoms that could be managed with symptomatic treatment to conditions such as posterior reversible encephalopathy syndrome and chronic inflammatory demyelinating polyradiculoneuropathy that may require more immediate intervention. This information was utilized in addition to clinical experience to compile potential management options for prevention and treatment of neurotoxic adverse events. This review is limited by the utilization of primarily retrospective studies and case reports. The available literature on the subject is largely narrative and there are no guidelines on treatment of tacrolimus-induced neurotoxicity at the time of this research. This comprehensive review may guide further studies to investigate the pathophysiology of tacrolimus-induced neurotoxicity and to define patient-specific strategies for mitigation or minimization of neurotoxicity. This is especially important given that management of tacrolimus-induced neurotoxicity can include changes to immunosuppression that can result in an increased risk of rejection.

BACKGROUND: During the past 3 years of the corona virus disease 2019 (COVID-19) pandemic, COVID-19 has been recognized to cause various neurological complications, including rare posterior reversible encephalopathy syndrome (PRES). In previously reported cases of PRES associated with COVID-19, the majority of patients had severe COVID-19 infection and known predisposing factors for PRES, such as uncontrolled hypertension, renal dysfunction, and use of immunosuppressants. It remains unclear whether these risk factors or infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) contributes to the development of PRES in these patients. Here we report a special case of PRES associated with COVID-19 without any known risk factors for PRES, indicating the SARS-CoV-2\'s direct role in the pathogenesis of PRES associated with COVID-19.
METHODS: An 18-year-old female patient presented to the emergency department with abdominal pain. Preliminary investigations showed no abnormalities, except for positive results in novel coronavirus nucleic acid tests using oropharyngeal swabs. However, the patient subsequently developed tonic-clonic seizures, headaches, and vomiting on the second day. Extensive investigations have been performed, including brain MRI and lumbar puncture. Brain MRI showed hypointense T1-weighted and hyperintense T2-weighted lesions in the bilateral occipital, frontal, and parietal cortices without enhancement effect. Blood and cerebrospinal fluid analyses yielded negative results. The patient had no hypertension, renal insufficiency, autoimmune disease, or the use of immunosuppressants or cytotoxic drugs.
METHODS: PRES was diagnosed based on the clinical features and typical MRI findings of PRES.
METHODS: Symptomatic treatments such as anticonvulsants were administered to the patients.
RESULTS: The patient fully recovered within 1 week. The initial MRI abnormalities also disappeared completely on a second MR examination performed 11 days later, supporting the diagnosis of PRES. The patient was followed up for 6 months and remained in a normal state.
CONCLUSIONS: The current case had no classical risk factors for PRES, indicating that although the cause of PRES in COVID-19 patients may be multifactorial, the infection of SARS-CoV-2 may play a direct role in the pathogenesis of PRES associated with COVID-19.

Posterior reversible encephalopathy syndrome (PRES) is a rare clinical disease, which has been seen in patients with systemic lupus erythematosus (SLE). Its main manifestations are seizure, headache and other neurological symptoms. While the condition is reversible, if not treated in time, there can be risks of cerebral haemorrhage. We report here the case of a young patient with SLE who developed PRES after receiving the immunosuppressant, mycophenolate mofetil. Neurological symptoms, signs, or changes in a patient\'s condition that cannot be explained by lupus, should alert physicians to the possibility of the drug causing PRES, and prompt discontinuation should ensue.

Hereditary renal hypouricemia (RHUC) is a heterogenous disorder characterized by defective uric acid (UA) reabsorption resulting in hypouricemia and increased fractional excretion of UA. RHUC is an important cause of exercise-induced acute kidney injury (EIAKI), nephrolithiasis and posterior reversible encephalopathy syndrome (PRES). We present here an unusual case of a patient with RHUC who presented with recurrent EIAKI and had two heterozygous mutations in the SLC2A9 gene.
A 43-year old man was admitted to our clinic because of bilateral loin pain, nausea and sleeplessness for 3 days after strenuous exercise. The laboratory results revealed increased levels of blood urea nitrogen (BUN) (15 mmol/l) and serum creatinine (Scr) (450 μmol/l), while the UA level was extremely low at 0.54 mg/dl, and his fractional excretion of urate (FE-UA) was 108%. The patient had an episode of acute kidney injury after playing soccer approximately 20 years ago, and on routine physical examination, his UA was less than 0.50 mg/dl. In view of the marked hypouricemia and high FE-UA, a diagnosis of RHUC was suspected, which led us to perform mutational screening of the SLC22A12 and SLC2A9 genes. DNA sequencing revealed no mutation in SLC22A12 gene, but two heterozygous mutations in the SLC2A9 gene.
This is a rare report of a patient with RHUC2 due to the mutation of SLC2A9. And this unique symptom of EIAKI and decreased or normal serum concentrations of UA warrant more attention as an early cue of RHUC.

Posterior reversible encephalopathy syndrome (PRES) is a clinical and radiological entity characterized by nonspecific symptomatology (eg, headache, visual disturbances, encephalopathy, and seizures) and classically cortical and subcortical vasogenic edema predominantly affecting the parietooccipital region. PRES etiologies are usually dichotomized into toxic PRES (eg, antineoplastic drugs, illicit drugs) and clinical condition-associated PRES (eg, acute hypertension, dysimmune disorders). Although the pathophysiology of PRES remains elusive, 2 main pathogenic hypotheses have been suggested: cerebral hyperperfusion due to acute hypertension and cerebral hypoperfusion related to endothelial dysfunction. Research into the pathogenesis of PRES has emerged through the development of animal models in the last decade. The motivation for developing a suitable PRES model is 2-fold: to fill in knowledge gaps of the pathophysiological mechanisms involved, and to open new perspectives for clinical assessment of pharmacological targets to improve therapeutic management of PRES. All current models of PRES have a hypertensive background, on which other triggers (acute hypertension, inflammatory, drug toxicity) have been added to address specific facets of PRES (eg, seizures). The initial model consisted in inducing a reduced uterine perfusion pressure that mimics preeclampsia, a leading cause of PRES. More recently, a model of stroke-prone spontaneously hypertensive rats on high-salt diet, originally developed for hypertensive small vessel disease and vascular cognitive impairment, has been studied in PRES. This review aims to discuss, depending on the research objective, the benefits and limitations of current experimental approaches and thus to define the desirable characteristics for studying the pathophysiology of PRES and developing new therapies.