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Systemic Lupus Erythematosus: HELP
Articles by Robin L. Brey
Based on 10 articles published since 2009
(Why 10 articles?)

Between 2009 and 2019, R. Brey wrote the following 10 articles about Lupus Erythematosus, Systemic.
+ Citations + Abstracts
1 Guideline European League Against Rheumatism recommendations for monitoring patients with systemic lupus erythematosus in clinical practice and in observational studies. 2010

Mosca, M / Tani, C / Aringer, M / Bombardieri, S / Boumpas, D / Brey, R / Cervera, R / Doria, A / Jayne, D / Khamashta, M A / Kuhn, A / Gordon, C / Petri, M / Rekvig, O P / Schneider, M / Sherer, Y / Shoenfeld, Y / Smolen, J S / Talarico, R / Tincani, A / van Vollenhoven, R F / Ward, M M / Werth, V P / Carmona, L. ·Correspondence to Dr Marta Mosca, University of Pisa, via Roma 67, Ospedale S. Chiara, Pisa, 56126, Italy. marta.mosca@int.med.unipi.it ·Ann Rheum Dis · Pubmed #19892750.

ABSTRACT: OBJECTIVES: To develop recommendations for monitoring patients with systemic lupus erythematosus (SLE) in clinical practice and observational studies and to develop a standardised core set of variables to monitor SLE. METHODS: We followed the European League Against Rheumatism (EULAR) standardised procedures for guideline development. The following techniques were applied: nominal groups, Delphi surveys for prioritisation, small group discussion, systematic literature review and two Delphi rounds to obtain agreement. The panel included rheumatologists, internists, dermatologists, a nephrologist and an expert related to national research agencies. The level of evidence and grading of recommendations were determined according to the Levels of Evidence and Grades of Recommendations of the Oxford Centre for Evidence-Based Medicine. RESULTS: A total of 10 recommendations have been developed, covering the following aspects: patient assessment, cardiovascular risk factors, other risk factors (osteoporosis, cancer), infection risk (screening, vaccination, monitoring), frequency of assessments, laboratory tests, mucocutaneous involvement, kidney monitoring, neuropsychological manifestations and ophthalmology assessment. A 'core set' of minimal variables for the assessment and monitoring of patients with SLE in clinical practice was developed that included some of the recommendations. In addition to the recommendations, indications for specific organ assessments that were viewed as part of good clinical practice were discussed and included in the flow chart. CONCLUSIONS: A set of recommendations for monitoring patients with SLE in routine clinical practice has been developed. The use of a standardised core set to monitor patients with SLE should facilitate clinical practice, as well as the quality control of care for patients with SLE, and the collection and comparison of data in observational studies.

2 Review Neurologic manifestations of systemic lupus erythematosus in children and adults. 2010

Muscal, Eyal / Brey, Robin L. ·Division of Pediatric Rheumatology, Texas Children's Hospital/Baylor College of Medicine, 6621 Fannin Street MC 3-2290, Houston, TX 77030, USA. ·Neurol Clin · Pubmed #19932376.

ABSTRACT: Among the collagen vascular diseases neurologic manifestations have been most commonly recognized and well-studied in systemic lupus erythematosus (SLE, lupus). Neurologic manifestations are less prevalent in other systemic inflammatory and autoimmune disorders. This review focuses on the clinical presentation, pathophysiology, and treatment strategies of neuropsychiatric lupus (NPSLE) in children and adults.

3 Article Anti-C1q antibodies in systemic lupus erythematosus. 2015

Orbai, A-M / Truedsson, L / Sturfelt, G / Nived, O / Fang, H / Alarcón, G S / Gordon, C / Merrill, Jt / Fortin, P R / Bruce, I N / Isenberg, D A / Wallace, D J / Ramsey-Goldman, R / Bae, S-C / Hanly, J G / Sanchez-Guerrero, J / Clarke, A E / Aranow, C B / Manzi, S / Urowitz, M B / Gladman, D D / Kalunian, K C / Costner, M I / Werth, V P / Zoma, A / Bernatsky, S / Ruiz-Irastorza, G / Khamashta, M A / Jacobsen, S / Buyon, J P / Maddison, P / Dooley, M A / Van Vollenhoven, R F / Ginzler, E / Stoll, T / Peschken, C / Jorizzo, J L / Callen, J P / Lim, S S / Fessler, B J / Inanc, M / Kamen, D L / Rahman, A / Steinsson, K / Franks, A G / Sigler, L / Hameed, S / Pham, N / Brey, R / Weisman, M H / McGwin, G / Magder, L S / Petri, M. ·Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. · Department of Laboratory Medicine, Section of Microbiology, Immunology and Glycobiology, Lund University, Lund, Sweden. · Department of Rheumatology, Skåne University Hospital, Lund, Sweden. · Department of Medicine, Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, Birmingham, AL, USA. · Rheumatology Research Group, School of Immunity and Infection, College of Medical and Dental Sciences University of Birmingham, Birmingham, UK. · Department of Clinical Pharmacology, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA. · Division of Rheumatology, Department of Medicine, Centre Hospitalier Universitaire (CHU) de Québec Axe Maladies Infectieuses et Immunitaires, CRCHU de Québec, Université Laval, Quebec City, Quebec, Canada. · Arthritis Research UK Centre for Epidemiology, Centre for Musculoskeletal Research, Institute of Inflammation and Repair, Manchester Academic Health Sciences Centre, The University of Manchester, Manchester, UK NIHR Manchester Musculoskeletal Biomedical Research Unit, Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, UK. · Centre for Rheumatology, Research Division of Medicine, London, UK. · Cedars-Sinai Medical Center, David Geffen School of Medicine, University of California, Los Angeles, CA, USA. · Northwestern University, Feinberg School of Medicine, Chicago, IL, USA. · Department of Rheumatology, Hanyang University Hospital for Rheumatic Diseases, Seoul, Korea. · Division of Rheumatology, Departments of Medicine and Pathology Capital Health and Dalhousie University, Halifax, Nova Scotia, Canada. · Mount Sinai Hospital and University Health Network, Toronto, Ontario, Canada. · Divisions of Clinical Epidemiology and Rheumatology, McGill University Health Centre, Montreal, Quebec, Canada. · Feinstein Institute for Medical Research, Manhasset, NY, USA. · Department of Medicine, Division of Rheumatology, Allegheny Singer Research Institute, Allegheny General Hospital, Pittsburgh, PA, USA. · Toronto Western Hospital Toronto, Ontario, Canada. · Division of Rheumatology, Allergy and Immunology, UCSD School of Medicine, La Jolla, CA, USA. · North Dallas Dermatology Associates, Dallas, TX, USA. · Philadelphia VA Medical Center and University of Pennsylvania, Philadelphia, PA, USA. · Lanarkshire Centre for Rheumatology and Hairmyres Hospital, East Kilbride, UK. · Autoimmune Diseases Research Unit, Hospital Universitario Cruces Universidad del Pais Vasco, Barakaldo, Spain. · Rayne Institute and St Thomas' Hospital London, UK. · Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark. · New York University, New York, NY, USA. · Ysbyty Gwynedd, Bangor, UK. · University of North Carolina, Chapel Hill, NC, USA. · Karolinska University Hospital, Stockholm, Sweden. · State University of New York, Downstate Medical Center, Brooklyn, NY, USA. · Kantonsspital Schaffhausen, Schaffhausen, Switzerland. · University of Manitoba Winnipeg, Manitoba, Canada. · Wake Forest University, Winston-Salem, NC, USA. · University of Louisville, Louisville, KY, USA. · Emory University, Atlanta, GA, USA. · Division of Rheumatology, Department of Internal Medicine, Istanbul Medical Faculty, Istanbul University, Istanbul, Turkey. · Medical University of South Carolina, Charleston, SC, USA. · NIHR Manchester Musculoskeletal Biomedical Research Unit, Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, UK. · Landspitali University Hospital, Reykjavik, Iceland. · University of Texas Health Science Center, San Antonio, TX, USA. · Cedars-Sinai Medical Center, Los Angeles, CA, USA. · Department of Epidemiology and Public Health, University of Maryland, Baltimore, MD, USA. · Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA MPetri@jhmi.edu. ·Lupus · Pubmed #25124676.

ABSTRACT: OBJECTIVE: Anti-C1q has been associated with systemic lupus erythematosus (SLE) and lupus nephritis in previous studies. We studied anti-C1q specificity for SLE (vs rheumatic disease controls) and the association with SLE manifestations in an international multicenter study. METHODS: Information and blood samples were obtained in a cross-sectional study from patients with SLE (n = 308) and other rheumatologic diseases (n = 389) from 25 clinical sites (84% female, 68% Caucasian, 17% African descent, 8% Asian, 7% other). IgG anti-C1q against the collagen-like region was measured by ELISA. RESULTS: Prevalence of anti-C1q was 28% (86/308) in patients with SLE and 13% (49/389) in controls (OR = 2.7, 95% CI: 1.8-4, p < 0.001). Anti-C1q was associated with proteinuria (OR = 3.0, 95% CI: 1.7-5.1, p < 0.001), red cell casts (OR = 2.6, 95% CI: 1.2-5.4, p = 0.015), anti-dsDNA (OR = 3.4, 95% CI: 1.9-6.1, p < 0.001) and anti-Smith (OR = 2.8, 95% CI: 1.5-5.0, p = 0.01). Anti-C1q was independently associated with renal involvement after adjustment for demographics, ANA, anti-dsDNA and low complement (OR = 2.3, 95% CI: 1.3-4.2, p < 0.01). Simultaneously positive anti-C1q, anti-dsDNA and low complement was strongly associated with renal involvement (OR = 14.9, 95% CI: 5.8-38.4, p < 0.01). CONCLUSIONS: Anti-C1q was more common in patients with SLE and those of Asian race/ethnicity. We confirmed a significant association of anti-C1q with renal involvement, independent of demographics and other serologies. Anti-C1q in combination with anti-dsDNA and low complement was the strongest serological association with renal involvement. These data support the usefulness of anti-C1q in SLE, especially in lupus nephritis.

4 Article Derivation and validation of the Systemic Lupus International Collaborating Clinics classification criteria for systemic lupus erythematosus. 2012

Petri, Michelle / Orbai, Ana-Maria / Alarcón, Graciela S / Gordon, Caroline / Merrill, Joan T / Fortin, Paul R / Bruce, Ian N / Isenberg, David / Wallace, Daniel J / Nived, Ola / Sturfelt, Gunnar / Ramsey-Goldman, Rosalind / Bae, Sang-Cheol / Hanly, John G / Sánchez-Guerrero, Jorge / Clarke, Ann / Aranow, Cynthia / Manzi, Susan / Urowitz, Murray / Gladman, Dafna / Kalunian, Kenneth / Costner, Melissa / Werth, Victoria P / Zoma, Asad / Bernatsky, Sasha / Ruiz-Irastorza, Guillermo / Khamashta, Munther A / Jacobsen, Soren / Buyon, Jill P / Maddison, Peter / Dooley, Mary Anne / van Vollenhoven, Ronald F / Ginzler, Ellen / Stoll, Thomas / Peschken, Christine / Jorizzo, Joseph L / Callen, Jeffrey P / Lim, S Sam / Fessler, Barri J / Inanc, Murat / Kamen, Diane L / Rahman, Anisur / Steinsson, Kristjan / Franks, Andrew G / Sigler, Lisa / Hameed, Suhail / Fang, Hong / Pham, Ngoc / Brey, Robin / Weisman, Michael H / McGwin, Gerald / Magder, Laurence S. ·Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 7500, Baltimore, MD 21205, USA. mpetri@jhmi.edu ·Arthritis Rheum · Pubmed #22553077.

ABSTRACT: OBJECTIVE: The Systemic Lupus International Collaborating Clinics (SLICC) group revised and validated the American College of Rheumatology (ACR) systemic lupus erythematosus (SLE) classification criteria in order to improve clinical relevance, meet stringent methodology requirements, and incorporate new knowledge regarding the immunology of SLE. METHODS: The classification criteria were derived from a set of 702 expert-rated patient scenarios. Recursive partitioning was used to derive an initial rule that was simplified and refined based on SLICC physician consensus. The SLICC group validated the classification criteria in a new validation sample of 690 new expert-rated patient scenarios. RESULTS: Seventeen criteria were identified. In the derivation set, the SLICC classification criteria resulted in fewer misclassifications compared with the current ACR classification criteria (49 versus 70; P = 0.0082) and had greater sensitivity (94% versus 86%; P < 0.0001) and equal specificity (92% versus 93%; P = 0.39). In the validation set, the SLICC classification criteria resulted in fewer misclassifications compared with the current ACR classification criteria (62 versus 74; P = 0.24) and had greater sensitivity (97% versus 83%; P < 0.0001) but lower specificity (84% versus 96%; P < 0.0001). CONCLUSION: The new SLICC classification criteria performed well in a large set of patient scenarios rated by experts. According to the SLICC rule for the classification of SLE, the patient must satisfy at least 4 criteria, including at least one clinical criterion and one immunologic criterion OR the patient must have biopsy-proven lupus nephritis in the presence of antinuclear antibodies or anti-double-stranded DNA antibodies.

5 Article Neuroimaging evidence of white matter inflammation in newly diagnosed systemic lupus erythematosus. 2011

Ramage, Amy E / Fox, Peter T / Brey, Robin L / Narayana, Shalini / Cykowski, Matthew D / Naqibuddin, Mohammad / Sampedro, Margaret / Holliday, Stephen L / Franklin, Crystal / Wallace, Daniel J / Weisman, Michael H / Petri, Michelle. ·University of Texas Health Science Center at San Antonio and Department of Veterans Affairs Heart of Texas Health Care Network, San Antonio, TX 78229, USA. ramagea@uthscsa.edu ·Arthritis Rheum · Pubmed #21618460.

ABSTRACT: OBJECTIVE: Central nervous system (CNS) involvement occurs frequently in systemic lupus erythematosus (SLE) and frequently results in morbidity. The primary pathophysiology of CNS involvement in SLE is thought to be inflammation secondary to autoantibody-mediated vasculitis. Neuroimaging studies have shown hypometabolism (representing impending cell failure) and atrophy (representing late-stage pathology), but not inflammation. The purpose of this study was to detect the presence and regional distribution of inflammation (hypermetabolism) and tissue failure, apoptosis, or atrophy (hypometabolism). METHODS: Eighty-five patients with newly diagnosed SLE, who had no focal neurologic symptoms, were studied. Disease activity was quantified using the Safety of Estrogens in Lupus Erythematosus: National Assessment version of the SLE Disease Activity Index (SELENA-SLEDAI), a validated index of SLE-related disease activity. 18Fluorodeoxyglucose (FDG) positron emission tomography (PET) images of glucose uptake were analyzed by visual inspection and as group statistical parametric images, using the SELENA-SLEDAI score as the analysis regressor. RESULTS: SELENA-SLEDAI-correlated increases in glucose uptake were found throughout the white matter, most markedly in heavily myelinated tracts. SELENA-SLEDAI-correlated decreases were found in the frontal and parietal cortex, in a pattern similar to that seen during visual inspection and presented in previous reports of hypometabolism. CONCLUSION: The SELENA-SLEDAI-correlated increases in glucose consumption are potential evidence of inflammation, consistent with prior reports of hypermetabolism in inflammatory disorders. To our knowledge, this is the first imaging-based evidence of SLE-induced CNS inflammation in an SLE inception cohort. The dissociation among 18FDG uptake characteristics, spatial distribution, and disease activity correlation is in accordance with the notion that glucose hypermetabolism and hypometabolism reflect fundamentally different aspects of the pathophysiology of SLE with CNS involvement.

6 Article Antiphospholipid antibodies and the brain: a consensus report. 2011

Brey, R L / Muscal, E / Chapman, J. ·University of Texas Health Science Center at San Antonio, Department of Neurology, San Antonio, TX 78229, USA. brey@uthscsa.edu ·Lupus · Pubmed #21303831.

ABSTRACT: This report discusses the difference between antiphospholipid antibodies (aPL) as a predictor for first and recurrent ischemic stroke, whether or not concomitant systemic lupus erythematosus (SLE) increases aPL-associated risk, and the association of aPL with other neurological manifestations. The neurological manifestations covered in this report were selected because they are among the most common, including cognitive dysfunction, headache, multiple sclerosis and seizures/epilepsy. Recommendations are made regarding further research that is needed to clarify remaining uncertainties.

7 Article International consensus for a definition of disease flare in lupus. 2011

Ruperto, N / Hanrahan, L M / Alarcón, G S / Belmont, H M / Brey, R L / Brunetta, P / Buyon, J P / Costner, M I / Cronin, M E / Dooley, M A / Filocamo, G / Fiorentino, D / Fortin, P R / Franks, A G / Gilkeson, G / Ginzler, E / Gordon, C / Grossman, J / Hahn, B / Isenberg, D A / Kalunian, K C / Petri, M / Sammaritano, L / Sánchez-Guerrero, J / Sontheimer, R D / Strand, V / Urowitz, M / von Feldt, J M / Werth, V P / Merrill, J T / Anonymous2840681. ·Gaslini Pediatria II, Reumatologia, PRINTO, Genova, Italy. ·Lupus · Pubmed #21148601.

ABSTRACT: The Lupus Foundation of America (LFA) convened an international working group to obtain a consensus definition of disease flare in lupus. With help from the Paediatric Rheumatology International Trials Organization (PRINTO), two web-based Delphi surveys of physicians were conducted. Subsequently, the LFA held a second consensus conference followed by a third Delphi survey to reach a community-wide agreement for flare definition. Sixty-nine of the 120 (57.5%) polled physicians responded to the first survey. Fifty-nine of the responses were available to draft 12 preliminary statements, which were circulated in the second survey. Eighty-seven of 118 (74%) physicians completed the second survey, with an agreement of 70% for 9/12 (75%) statements. During the second conference, three alternative flare definitions were consolidated and sent back to the international community. One hundred and sixteen of 146 (79.5%) responded, with agreement by 71/116 (61%) for the following definition: "A flare is a measurable increase in disease activity in one or more organ systems involving new or worse clinical signs and symptoms and/or laboratory measurements. It must be considered clinically significant by the assessor and usually there would be at least consideration of a change or an increase in treatment." The LFA proposes this definition for lupus flare on the basis of its high face validity.

8 Article Depression and cognitive impairment in newly diagnosed systemic lupus erythematosus. 2010

Petri, Michelle / Naqibuddin, Mohammad / Carson, Kathryn A / Wallace, Daniel J / Weisman, Michael H / Holliday, Stephen L / Sampedro, Margaret / Padilla, Patricia A / Brey, Robin L. ·Johns Hopkins University, Suite 7500, Baltimore, Maryland 21205, USA. mpetri@jhmi.edu ·J Rheumatol · Pubmed #20634244.

ABSTRACT: OBJECTIVE: Cognitive impairment is present in 80% of patients with systemic lupus erythematosus (SLE) 10 years after diagnosis. The natural history of cognitive dysfunction in newly diagnosed SLE is unknown. We examined the association of depression and cognitive performance in newly diagnosed SLE. METHODS: A multicenter cohort of 111 patients newly diagnosed (within 9 months) with SLE underwent cognitive function testing using an automated battery [Automated Neuropsychological Assessment Metrics (ANAM)] with 9 subtests. Depression was measured using the Calgary Depression Scale (CDS). RESULTS: The patient cohort was 97.3% female, 55.9% white, 15.3% African American, 20.7% Hispanic, mean age 37.8 years, mean education 15.2 years. CDS score ranged from 0 to 18 (mean 5.0 ± 4.6). CDS score did not differ by age, sex, ethnicity, or prednisone dose. Higher Krupp Fatigue Severity Scale scores and presence of fibromyalgia were significantly associated with higher CDS score (p < 0.001; p = 0.006, respectively). Depressed patients, defined by a CDS score > 6, had significantly poorer performance on 5 ANAM throughput measures: code substitution (p = 0.03), continuous performance (p = 0.02), matching-to-sample (p = 0.04), simple reaction time (p = 0.02), and the Sternberg memory test (p = 0.04). Adjusting for age, sex, ethnicity, education, and prednisone dose, a higher CDS score remained significantly associated with poorer performance on 3 measures, but the association was slightly attenuated for code substitution and matching-to-sample. Depression was not associated with mathematical or spatial processing. CONCLUSION: Depression, a modifiable risk factor, is associated with significantly poorer function in several cognitive domains in patients newly diagnosed with SLE. Treatment of depression when the CDS score is greater than 6 may improve cognitive functioning and should be further studied.

9 Article Cerebral and cerebellar volume loss in children and adolescents with systemic lupus erythematosus: a review of clinically acquired brain magnetic resonance imaging. 2010

Muscal, Eyal / Traipe, Elfrides / de Guzman, Marietta M / Myones, Barry L / Brey, Robin L / Hunter, Jill V. ·Baylor College of Medicine and Pediatric Rheumatology Center, Houston, TX 77030, USA. emuscal@bcm.tmc.edu ·J Rheumatol · Pubmed #20516022.

ABSTRACT: OBJECTIVE: Cerebral atrophy is a prominent feature in adults with systemic lupus erythematosus (SLE). We assessed cerebral and cerebellar volume loss on clinically acquired brain magnetic resonance imaging (MRI) scans of children and adolescents with SLE. METHODS: We abstracted information on disease course for patients who underwent clinical brain MRI during the period 2002-2008. We completed qualitative assessments of volume loss and measured corpus callosum thickness and ventricular enlargement for patients with lupus and controls. RESULTS: Forty-nine children underwent brain MRI during the review period due to clinical indications. The lupus cohort was predominantly female and ethnically diverse. Mean age at imaging was 15.3 +/- 2.6 years and mean disease duration was 30.6 +/- 33.3 months. Findings suggestive of cerebral and cerebellar volume loss were seen respectively in 89.8% and 91.8% of lupus patients. Cerebral volume loss was moderate or severe in 26.5% of children. Cerebellar volume loss was moderate in 20.4% of these patients. Linear measurement means reflected corpus callosum thinning and ventricular enlargement in lupus patients. Volume loss was observed in newly diagnosed patients prior to corticosteroid use. Disease duration and corticosteroid use did not predict the severity of volume loss. There were statistically significant differences in linear imaging measurements comparing lupus patients to 14 similar-age controls. CONCLUSION: Regional volume loss was observed in most adolescents with lupus undergoing clinical brain MRI scans. As in other pediatric conditions with inflammatory or vascular etiologies, these findings may be reflecting disease-associated neuronal loss and not solely the effects of corticosteroid.

10 Article MR imaging findings suggestive of posterior reversible encephalopathy syndrome in adolescents with systemic lupus erythematosus. 2010

Muscal, Eyal / Traipe, Elfrides / de Guzman, Marietta M / Myones, Barry L / Brey, Robin L / Hunter, Jill V. ·Baylor College of Medicine and Pediatric Rheumatology Center, Texas Children's Hospital, 6621 Fannin St., MC 3-2290, Houston, TX 77030, USA. emuscal@bcm.tmc.edu ·Pediatr Radiol · Pubmed #20119723.

ABSTRACT: BACKGROUND: Endothelial damage, hypertension and cytotoxic medications may serve as risk factors for the posterior reversible encephalopathy syndrome (PRES) in systemic lupus erythematosus. There have been few case reports of these findings in pediatric lupus patients. OBJECTIVE: We describe clinical and neuroimaging findings in children and adolescents with lupus and a PRES diagnosis. MATERIALS AND METHODS: We identified all clinically acquired brain MRIs of lupus patients at a tertiary care pediatric hospital (2002-2008). We reviewed clinical features, conventional MRI and diffusion-weighted imaging (DWI) findings of patients with gray- and white-matter changes suggestive of vasogenic edema and PRES. RESULTS: Six pediatric lupus patients presenting with seizures and altered mental status had MRI findings suggestive of PRES. In five children clinical and imaging changes were seen in conjunction with hypertension and active renal disease. MRI abnormalities were diffuse and involved frontal regions in five children. DWI changes reflected increased apparent diffusivity coefficient (unrestricted diffusion in all patients). Clinical and imaging changes significantly improved with antihypertensive and fluid management. CONCLUSION: MRI changes suggestive of vasogenic edema and PRES may be seen in children with active lupus and hypertension. The differential diagnosis of seizures and altered mental status should include PRES in children, as it does in adults.