This article has Open Peer Review reports available.
Posterior reversible encephalopathy syndrome could be an underestimated variant of “reversible neurological deficits” in Systemic Lupus Erythematosus
© Liu et al.; licensee BioMed Central Ltd. 2012
Received: 12 May 2012
Accepted: 19 November 2012
Published: 5 December 2012
Posterior reversible encephalopathy syndrome (PRES) has been increasingly identified in patients with systemic lupus erythematosus (SLE) owing to the advance in neuroimaging techniques. Prompt diagnosis is pivotal to improve its outcome. To analyze the clinical and radiographic profile of PRES in patients with SLE and search for the appropriate treatment strategy PRES in SLE.
SLE patients who fulfilled the diagnostic criteria for PRES from August 2008 to January 2011 were evaluated at baseline, and followed to determine clinical outcomes. Data were analysis on clinical characteristics, laboratory abnormalities, treatment details, and outcomes.
Ten episodes of PRES in patients with SLE were identified. All patients were female, mean age of onset was 22.93 ± 2.48 years, and SLEDAI at the onset of PRES were 25.8 ± 5.7. All cases had acute onset of headache, altered mental status, stupor, vomiting, cortical blindness and seizures. Neurological symptoms were the initial manifestation of SLE in three cases. Head magnetic resonance imaging (MRI) demonstrated posterior white matter edema involving the parietal, temporal and occipital lobes, which were more conspicuous on T2 weighted spin echo and diffusion-weighted MR imaging (DWI) than on computed tomography (CT) scan. Complete clinical and radiographic recovery was observed in 8 patients after prompt treatment with corticosteroids.
PRES might be due to lupus per se besides other traditional causative factors such as hypertension. PRES might be an underestimated variant of “reversible neurological deficits” in SLE. Prompt recognition and timely management is important to prevent permanent neurological deficits.
KeywordsSystemic lupus erythematosus Neuropsychiatric lupus Posterior reversible encephalopathy syndrome
Systemic lupus erythematosus (SLE) is an autoimmune disease that can affect the central nervous system (CNS) . Neuropsychiatric manifestations vary from severe neurological and psychiatric disorders to more subtle signs such as headache, mood disorders and defects in cognitive function [2–6]. The presentations as well as the underlying immunopathogenic mechanisms can be heterogeneous and therefore pose diagnostic and therapeutic dilemmas.
Posterior reversible encephalopathy syndrome (PRES) was first reported by Aisen et al. in 1985 , which was a clinical entity characterized by headache, nausea, vomiting, seizures, conscious disturbance and visual disorder with predominantly white matter abnormalities of the parieto-occipital lobes on neuroimaging [8, 9]. PRES could be associated with several conditions, including hypertensive encephalopathy, eclampsia, immunosuppressive drugs and inflammatory disorders, and was reversible if treated promptly [8–12]. Literature review showed that severe hypertension (> 170/110 mmHg) and renal failure were present in the majority of previously reported cases of SLE with PRES, whereas SLE patients might also develop reversible focal deficits that respond to steroid therapy . The peculiar role of SLE itself in the occurrence of PRES was not clear since PRES could be a manifestation of lupus disease activity or a consequence of immunomodulatory therapy, making the diagnosis and treatment challenging. With the development of MRI techniques, there was a high likelihood of presentation of PRES to a rheumatologist. It was important to recognize the condition early in order to minimize potential for irreversible central nervous system damage.
Here, we analyzed the clinical data of 10 cases of SLE with PRES, systematically reviewed the pathogenesis and treatment patients with SLE-associated PRES reported in the literature. The aims of the present study were to reveal the relationship between PRES and SLE, to search for the appropriate treatment strategy PRES in SLE.
We studied the clinical data and neuroimaging of SLE patients with CNS involvement followed in department of Rheumatology of affiliated hospital Qingdao University Medical College from August 2008 to January 2011. Only SLE patients with PRES were selected, diagnosed according to the clinical and neuroradiological criteria reported in the literature. The abnormalities on imaging were defined as multiple cortico-subcortical areas of low white-matter attenuation on CT scans and as T1-weighted hypointense and T2-weighted hyperintense areas on MRI scans involving the occipital and parietal lobes bilaterally that had partially or completely resolved on follow-up scanning, when subsequent images were available. The clinical symptoms also tended to almost complete resolution after treatment [8, 9]. MRI and/or CT of patients showed normal despite pronounced neuropsychiatric symptoms, and repeat MRI should be done within 2 weeks. All patients fulfilled the American College of Rheumatology (ACR) classification criteria for SLE , and disease activity at the time of the PRES episode was calculated using SLE Disease Activity Index (SLEDAI) . Non-SLE patients, hypertensive encephalopathy, uremic encephalopathy, ischemic stroke and CNS infection were ruled out.
A brain MRI was performed with a 1.5 T GE Vectra and a standard head coil. Fast-Spin-echo T2-weighted (TR/TE/numbers of excitation = 2800/102/2), Spinecho PD-weighted (3000/40/2), Fast-Spin-echo T1-FLAIR-weighted (TR/TI/TE/numbers of excitation = 1750/720/15/2), and T2-FLAIR-weighted (TR/TI/TE/numbers of excitation = 8400/2100/125/1) sequences were performed in the axial and coronal planes, with 5 mm slice thickness. The imaging sequence for DWI was single-shot spinecho echo-planar imaging (4600/≥30 repetition time/echo time) with diffusion sensitivities b = 0 and b = 1,000 s/mm2. The diffusion gradients were applied sequentially in three orthogonal directions to generate three sets of axial diffusion-weighted MR imaging (DWI). Sections (5 mm thick) with 1.5 mm interslice gaps, 24 cm field of view, and 128 × 130 matrix were used for all scans. The scan time was 40 s. A composite isotropic trace image was made by multiplying the three DWI together and taking the cubic root of the result to remove the effects of diffusion anisotropy. Interpretations were made using three sets of DWI and the composite isotropic trace image. A non-contrast CT scan (Sensation 64, Siemens, Erlangen, Germany) was also available in two cases. All studies were evaluated by two expert neuroradiologists.
This study protocol was approved by the Research Ethics Committee of The Affiliation Hospital of QingDao University Medical College and followed the ethical guidelines of the 1975 Declaration of Helsinki and subsequent ones . All patients gave written informed consent to participate in this study.
Patient characteristics and clinical presentations
Clinical and laboratory characteristics
10 episodes, no. (%)
Age at onset (years)
22.93 ± 2.48 *
20.8 ± 12.8*
25.8 ± 5.7*
Associated risk factors
Renal failure (cr. ≥1.5 mg/dl) b
Complete neurological recovery
Residual neurological deficit
Patients with positive serum anti-SSA, anti-SSB, anti-dsDNA, antiphospholipid (aPL), anti-RNP/Sm, anti-Sm and anti-Nucleosome antibodies were 7/10, 2/10, 6/10, 4/10, 3/10, 2/10, 2/10, respectively. Eight patients (80%) had a history of new or previously diagnosis lupus nephritis, hypoproteinemia as well as hypocomplementemia, and 2 had renal incompetency. All patients had activated disease at onset of PRES (SLEDAI range 13–38). Lumbar puncture was carried on 8 patients, and two patients were demonstrated opening pressure beyond 180mm H2O. Cerebrospinal fluid examination revealed no abnormality (normal protein and glucose concentration with negative pathogenic finding).
10 episodes, no. (%)
High signal DWI
Treatment and outcome
Eight patients were treated with methylprednisolone pulses (1 g/day for 3 days) as well as intravenous gamma-globulin (400mg g/kg/day for 3 days) followed by oral prednisone (0.5–1.0mg/kg/day). After pulse treatment, eight patients were treated with cyclophosphamide (400mg/m2/week). Two patients were treated with methylprednisolone (1.0mg/kg/day) during acute phase in the department of emergency. For those patients with acute hypertension, potent antihypertensive therapy was instituted as well as general supportive measures.
Complete clinic-neruroradiographic recovery occurred in 8 patients after treatment. One patient resulted in refractory vomiting due to delayed diagnosis and therapy, notwithstanding neruroradiographic recovery at followup. One patient died of the acute episode of SLE.
Discussion and conclusions
With advance in neuroimaging techniques, PRES has been accumulating identified over the past decade [8, 17]. The similarities of the clinical manifestations between PRES, neuropsychiatric SLE (NPSLE) and lupus-related complications CNS, such as CNS infection and psychiatric conditions, often pose a diagnostic and therapeutic challenge for rheumatologist. The differential diagnosis between these entities is important, as the first requires immunosuppressive therapy, which should be avoided in the later situation [18, 19].
The exact pathophysiological mechanism of PRES remains uncertain . To date, three hypotheses have been proposed, which include: (i) cerebral vasoconstriction with subsequent infarcts of the brain, (ii) failure of cerebral autoregulation with consequent vasogenic oedema, and (iii) endothelial damage with disruption of the blood–brain barrier causing fluid and protein transudation in the brain [8, 20–22]. The pathophysiology of PRES in SLE is also less well understood. In most cases of SLE-related PRES, immunosuppresants used to treat the SLE were suggested as causative factors, though lupus itself or SLE-related hypertension, antiphospholipid antibodies or renal failure might also be contributive. Abnormal endothelial activation, dysfunction and leukocyte tracking have recently been documented to cause brain and systemic hypoperfusion, which may be causative factors for PRES in SLE [21, 23–30].
On the other hand, endothelial cell activation is one of the pathogenic hallmarks of NPSLE. It usually occurs after exposure to interleukin 1 (IL-1) and TNF-α, and may be enhanced by local release of IL-1 and IL-6 . SLE patients with high SLEDAI have increased serum levels of TNF-α and other pro-inflammatory cytokines that may stimulate endothelial cells of intracranial vessels and astrocytes to produce nitric oxide (NO), causing blood–brain barrier (BBB) damage and plasma leakage . In some cases the endothelial dysfunction together with hemodynamic factors may allow the escape of blood plasma and large amounts of red blood cells resulting in secondary parenchymal hematoma . Histopathology showed the PRES manifestation result from NPSLE were due to focal cerebral edema associated with blood vessel injury and ischemic changes, although in many cases histopathology did not demonstrate specific lesions .
The occurrence of autoantibodies to SSA have been linked with vasculitis, and aPL have been involved in abnormal endothelial activation [33–35]. Our study also showed that the occurrence of anti-SSA antibodies, hypoproteinemia and hypocomplementemia might be associated with PRES. Accordingly the cause of PRES in SLE was probably due to multiple factors including lupus disease activity, hypertension, nephritis, and/or medications. Most reports had ascribed various immunosuppressive medications as causative factors. However SLE patients who were in need of immunosuppressants treatment often had active and severe disease [25, 27, 36], PRES could also occur in new-onset, activity SLE as well as an absolute increase in blood pressure . Furthermore our series had one main distinguishing feature compared with the available literature: only 3 patients presented with severe hypertension (> 170/110 mmHg) including 2 patients had severity hypertension after the onset of PRES, compared with 95% in the reported literature. A cytotoxic effect of SLE could explain why PRES might occur in the absence of severe hypertension [11, 37–39]. Consequently PRES might develop as the initial manifestation of SLE per se instead of complication of medications.
The typical MRI features of PRES are diffuse hyperintensities on T2-weighted and fluid attenuated inversion recovery (FLAIR) images in the white matter in the posterior areas of the cerebral hemispheres, which spare the calcarine and paramedian occipital lobe structures and are reversible . In recent years, another MR technique, echoplanar DWI findings are used in the diagnosis of PRES . Regions with vasogenic edema show marked hyperintensity on apparent diffusion coefficient (ADC) and mostly iso or hypointensity on DWI [27, 51]. Lack of restricted diffusion on the ADC map elaborated from DWI suggested potential reversibility. DWI can further aid in distinguishing vasogenic edema in PRES from the cytotoxic edema associated with early infracts. Cytotoxic edema has high signal intensity on DWI, due to decreased ADC, while vasogenic edema has low to intermediate signal intensity . Nevertheless the lesions of some patients challenge with this knowledge, an increase in T2 signal within regions of vasogenic edema could cause slight DW1 hyperintensity [52–54]. The extent of combined T2 and DWI signal abnormalities associated with patient outcome . However, whether DWI was specific in the diagnosis of patients with PRES remain to be determined . Thus the exact changes detected by use of DWI in patients with PRES should be further investigation
The management of PRES in SLE is dependent on etiology. In hypertension-related and drug-induced PRES, the key to effective therapeutic includes prompt withdraw of offending agent aggressive control of blood pressure, timely anti-convulsive therapy of seizures and temporary renal support. Whereas for SLE related PRES, vigorous treatment with corticosteroids plus cyclophosphamide is directed by lupus-related major organ manifestations. Although PRES is reversible once treatment is instituted, delayed diagnosis and therapy may lead to death or irreversible neurological deficit, as also shown in our series [11, 37, 38]. Therefore prompt recognition and timely rational management is important to prevent permanent neurological deficits. Nevertheless controversy still exist whether immunosuppression should be used in the treatment of PRES in SLE, randomized controlled trials should be performed for addressing the strategies of therapy the situation.
In conclusion, PRES is not an exceptional condition and might be an underestimated variant of “reversible neurological deficits” in SLE. With advances in radiologic imaging, there is a high likelihood of presentation of this syndrome to a rheumatologist. Whether PRES is a presenting manifestation of SLE disease activity and of its treatment or whether it represents a neurological symptoms of SLE remain to be determined. It is important to recognize the condition early in order to ensure a very high chance of total neurological recovery in SLE patients with PRES.
This work was supported by National Key Technology R&D Program in the 11th Five year Plan of China (No.2008BAI59B03)
- Omdal R, Mellgren SI, Husby G: Clinical neuropsychiatric and neuromuscular manifestations in systemic lupus erythematosus. Scand J Rheumatol. 1988, 17 (2): 113-117. 10.3109/03009748809098770.View ArticlePubMedGoogle Scholar
- Carbotte RM, Denburg SD, Denburg JA, Nahmias C, Garnett ES: Fluctuating cognitive abnormalities and cerebral glucose metabolism in neuropsychiatric systemic lupus erythematosus. J Neurol Neurosurg Psychiatry. 1992, 55 (11): 1054-1059. 10.1136/jnnp.55.11.1054.View ArticlePubMedPubMed CentralGoogle Scholar
- West SG: Neuropsychiatric lupus. Rheum Dis Clin North Am. 1994, 20 (1): 129-158.PubMedGoogle Scholar
- Chinn RJ, Wilkinson ID, Hall-Craggs MA, Paley MN, Shortall E, Carter S, et al: Magnetic resonance imaging of the brain and cerebral proton spectroscopy in patients with systemic lupus erythematosus. Arthritis Rheum. 1997, 40 (1): 36-46. 10.1002/art.1780400107.View ArticlePubMedGoogle Scholar
- Sanna G, Bertolaccini ML, Cuadrado MJ, Laing H, Khamashta MA, Mathieu A, et al: Neuropsychiatric manifestations in systemic lupus erythematosus: prevalence and association with antiphospholipid antibodies. J Rheumatol. 2003, 30 (5): 985-992.PubMedGoogle Scholar
- Sibbitt WL, Schmidt PJ, Hart BL, Brooks WM: Fluid Attenuated Inversion Recovery (FLAIR) imaging in neuropsychiatric systemic lupus erythematosus. J Rheumatol. 2003, 30 (9): 1983-1989.PubMedGoogle Scholar
- Aisen AM, Gabrielsen TO, McCune WJ: MR imaging of systemic lupus erythematosus involving the brain. Ajr. 1985, 144 (5): 1027-1031.View ArticlePubMedGoogle Scholar
- Hinchey J, Chaves C, Appignani B, Breen J, Pao L, Wang A, et al: A reversible posterior leukoencephalopathy syndrome. N Engl J Med. 1996, 334 (8): 494-500. 10.1056/NEJM199602223340803.View ArticlePubMedGoogle Scholar
- Casey SO, Sampaio RC, Michel E, Truwit CL: Posterior reversible encephalopathy syndrome: utility of fluid-attenuated inversion recovery MR imaging in the detection of cortical and subcortical lesions. Ajnr. 2000, 21 (7): 1199-1206.PubMedGoogle Scholar
- Lanzino G, Cloft H, Hemstreet MK, West K, Alston S, Ishitani M: Reversible posterior leukoencephalopathy following organ transplantation. Description of two cases. Clin Neurol Neurosurg. 1997, 99 (3): 222-226. 10.1016/S0303-8467(97)00028-0.View ArticlePubMedGoogle Scholar
- Servillo G, Striano P, Striano S, Tortora F, Boccella P, De Robertis E, et al: Posterior reversible encephalopathy syndrome (PRES) in critically ill obstetric patients. Intensive Care Med. 2003, 29 (12): 2323-2326. 10.1007/s00134-003-1901-1.View ArticlePubMedGoogle Scholar
- Magnano MD, Bush TM, Herrera I, Altman RD: Reversible posterior leukoencephalopathy in patients with systemic lupus erythematosus. Semin Arthritis Rheum. 2006, 35 (6): 396-402. 10.1016/j.semarthrit.2006.01.002.View ArticlePubMedGoogle Scholar
- Kimura M, Aramaki K, Wada T, Nishi K, Matsushita R, Iizuka N, et al: Reversible focal neurological deficits in systemic lupus erythematosus: report of 2 cases and review of the literature. J Neurol Sci. 2008, 272 (1–2): 71-76.View ArticlePubMedGoogle Scholar
- Hochberg MC: Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum. 1997, 40 (9): 1725-View ArticlePubMedGoogle Scholar
- Bombardier C, Gladman DD, Urowitz MB, Caron D, Chang CH: Derivation of the SLEDAI. A disease activity index for lupus patients. The Committee on Prognosis Studies in SLE. Arthritis Rheum. 1992, 35 (6): 630-640. 10.1002/art.1780350606.View ArticlePubMedGoogle Scholar
- Puri KS, Suresh KR, Gogtay NJ, Thatte UM: Declaration of Helsinki, 2008: implications for stakeholders in research. J Postgrad Med. 2009, 55 (2): 131-134. 10.4103/0022-3859.52846.View ArticlePubMedGoogle Scholar
- Casali-Rey JI, Davalos EG, Lopez-Amalfara A, Julio-Munoz D, Pagano MA: Posterior reversible encephalopathy syndrome: some case reports. Rev Neurol. 2003, 37 (3): 224-227.PubMedGoogle Scholar
- Fugate JE, Claassen DO, Cloft HJ, Kallmes DF, Kozak OS, Rabinstein AA: Posterior reversible encephalopathy syndrome: associated clinical and radiologic findings. Mayo Clin Proc. 2010, 85 (5): 427-432. 10.4065/mcp.2009.0590. MayView ArticlePubMedPubMed CentralGoogle Scholar
- Zhang YX, Liu JR, Ding MP, Huang J, Zhang M, Jansen O, et al: Reversible posterior encephalopathy syndrome in systemic lupus erythematosus and lupus nephritis. Internal medicine (Tokyo, Japan). 2008, 47 (9): 867-875. 10.2169/internalmedicine.47.0741.View ArticleGoogle Scholar
- Vaughan CJ, Delanty N: Hypertensive emergencies. Lancet. 2000, 356 (9227): 411-417. 10.1016/S0140-6736(00)02539-3.View ArticlePubMedGoogle Scholar
- Shin KC, Choi HJ, Bae YD, Lee JC, Lee EB, Song YW: Reversible posterior leukoencephalopathy syndrome in systemic lupus erythematosus with thrombocytopenia treated with cyclosporine. J Clin Rheumatol. 2005, 11 (3): 164-166. 10.1097/01.rhu.0000164825.63063.43.View ArticlePubMedGoogle Scholar
- Min L, Zwerling J, Ocava LC, Chen IH, Putterman C: Reversible posterior leukoencephalopathy in connective tissue diseases. Semin Arthritis Rheum. 2006, 35 (6): 388-395. 10.1016/j.semarthrit.2006.01.003.View ArticlePubMedGoogle Scholar
- Primavera A, Audenino D, Mavilio N, Cocito L: Reversible posterior leucoencephalopathy syndrome in systemic lupus and vasculitis. Ann Rheum Dis. 2001, 60 (5): 534-537. 10.1136/ard.60.5.534.View ArticlePubMedPubMed CentralGoogle Scholar
- Von Feldt JM: Reversible posterior leukoencephalopathy syndrome in systemic lupus erythematosus: what can this teach us?. J Clin Rheumatol. 2005, 11 (3): 127-128. 10.1097/01.rhu.0000166666.94382.e6.View ArticlePubMedGoogle Scholar
- Kur JK, Esdaile JM: Posterior reversible encephalopathy syndrome–an underrecognized manifestation of systemic lupus erythematosus. J Rheumatol. 2006, 33 (11): 2178-2183.PubMedGoogle Scholar
- Ishimori ML, Pressman BD, Wallace DJ, Weisman MH: Posterior reversible encephalopathy syndrome: another manifestation of CNS SLE?. Lupus. 2007, 16 (6): 436-443. 10.1177/0961203307078682.View ArticlePubMedGoogle Scholar
- Baizabal-Carvallo JF, Barragan-Campos HM, Padilla-Aranda HJ, Alonso-Juarez M, Estanol B, Cantu-Brito C, et al: Posterior reversible encephalopathy syndrome as a complication of acute lupus activity. Clin Neurol Neurosurg. 2009, 111 (4): 359-363. 10.1016/j.clineuro.2008.11.017.View ArticlePubMedGoogle Scholar
- Sibbitt WL, Brooks WM, Kornfeld M, Hart BL, Bankhurst AD, Roldan CA: Magnetic Resonance Imaging and Brain Histopathology in Neuropsychiatric Systemic Lupus Erythematosus. Semin Arthritis Rheum. 2010, 40 (1): 32-52. 10.1016/j.semarthrit.2009.08.005. AugView ArticlePubMedGoogle Scholar
- Bandettini di Poggio M, Murdaca G, Puppo F, Primavera A: Antiphospholipid Syndrome and Reversible Posterior Leukoencephalophaty Syndrome. Semin Arthritis Rheum. 2010, 40 (3): e9-10. 10.1016/j.semarthrit.2009.08.004. DecView ArticlePubMedGoogle Scholar
- Bag AK, Cure JK, Sullivan JC, Roberson GH: Central variant of posterior reversible encephalopathy syndrome in systemic lupus erythematosus: new associations?. Lupus. 2010, 19 (2): 225-226. 10.1177/0961203309345749.View ArticlePubMedGoogle Scholar
- Abbott NJ, Mendonca LL, Dolman DE: The blood–brain barrier in systemic lupus erythematosus. Lupus. 2003, 12 (12): 908-915. 10.1191/0961203303lu501oa.View ArticlePubMedGoogle Scholar
- Lee SC, Dickson DW, Liu W, Brosnan CF: Induction of nitric oxide synthase activity in human astrocytes by interleukin-1 beta and interferon-gamma. J Neuroimmunol. 1993, 46 (1–2): 19-24.View ArticlePubMedGoogle Scholar
- Alexander EL, Arnett FC, Provost TT, Stevens MB: Sjogren's syndrome: association of anti-Ro(SS-A) antibodies with vasculitis, hematologic abnormalities, and serologic hyperreactivity. Ann Intern Med. 1983, 98 (2): 155-159.View ArticlePubMedGoogle Scholar
- Molina R, Provost TT, Alexander EL: Two types of inflammatory vascular disease in Sjogren's syndrome. Differential association with seroreactivity to rheumatoid factor and antibodies to Ro (SS-A) and with hypocomplementemia. Arthritis Rheum. 1985, 28 (11): 1251-1258. 10.1002/art.1780281109.View ArticlePubMedGoogle Scholar
- Meroni PL, Raschi E, Camera M, Testoni C, Nicoletti F, Tincani A, et al: Endothelial activation by APL: a potential pathogenetic mechanism for the clinical manifestations of the syndrome. J Autoimm. 2000, 15: 237-240. 10.1006/jaut.2000.0412.View ArticleGoogle Scholar
- Mak A, Chan BP, Yeh IB, Ho RC, Boey ML, Feng PH, et al: Neuropsychiatric lupus and reversible posterior leucoencephalopathy syndrome: a challenging clinical dilemma. Rheumatology (Oxford). 2008, 47 (3): 256-262.View ArticleGoogle Scholar
- Kwon S, Koo J, Lee S: Clinical spectrum of reversible posterior leukoencephalopathy syndrome. Pediatr Neurol. 2001, 24 (5): 361-364. 10.1016/S0887-8994(01)00265-X.View ArticlePubMedGoogle Scholar
- Antunes NL, Small TN, George D, Boulad F, Lis E: Posterior leukoencephalopathy syndrome may not be reversible. Pediatr Neurol. 1999, 20 (3): 241-243. 10.1016/S0887-8994(98)00148-9.View ArticlePubMedGoogle Scholar
- Varaprasad IR, Agrawal S, Prabu VN, Rajasekhar L, Kanikannan MA, Narsimulu G: Posterior reversible encephalopathy syndrome in systemic lupus erythematosus. J Rheumatol. 2011, 38 (8): 1607-1611. 10.3899/jrheum.101308. AugView ArticlePubMedGoogle Scholar
- Shintani S, Ono K, Hinoshita H, Shiigai T, Tsuruoka S: Unusual neuroradiological findings in systemic lupus erythematosus. Eur Neurol. 1993, 33 (1): 13-16. 10.1159/000116891.View ArticlePubMedGoogle Scholar
- Zapor M, Rennie T, Murphy FT, Battafarano DF: Clinical images: neuropsychiatric systemic lupus erythematosus. Arthritis Rheum. 2000, 43 (9): 2045-PubMedGoogle Scholar
- Hanyuda M, Yoda Y, Shiozawa T, Hanaoka R, Miwa Y, Kaga S, et al: A case with systemic lupus erythematosus presenting with reversible edematous lesion in cerebellum. Ryumachi. 2002, 42 (5): 801-806.PubMedGoogle Scholar
- Sanders TG, Clayman DA, Sanchez-Ramos L, Vines FS, Russo L: Brain in eclampsia: MR imaging with clinical correlation. Radiology. 1991, 180 (2): 475-478.View ArticlePubMedGoogle Scholar
- Schwartz RB, Jones KM, Kalina P, Bajakian RL, Mantello MT, Garada B, et al: Hypertensive encephalopathy: findings on CT, MR imaging, and SPECT imaging in 14 cases. Ajr. 1992, 159 (2): 379-383.View ArticlePubMedGoogle Scholar
- De Klippel N, Sennesael J, Lamote J, Ebinger G, de Keyser J: Cyclosporin leukoencephalopathy induced by intravenous lipid solution. Lancet. 1992, 339 (8801): 1114-View ArticlePubMedGoogle Scholar
- Chou MC, Lai PH, Yeh LR, Li JY, Yuan MK, Liang HL, et al: Posterior reversible encephalopathy syndrome: magnetic resonance imaging and diffusion-weighted imaging in 12 cases. Kaohsiung J Med Sci. 2004, 20 (8): 381-388. 10.1016/S1607-551X(09)70174-3.View ArticlePubMedGoogle Scholar
- Gocmen R, Ozgen B, Oguz KK: Widening the spectrum of PRES: series from a tertiary care center. Eur J Radiol. 2007, 62 (3): 454-459. 10.1016/j.ejrad.2006.12.001.View ArticlePubMedGoogle Scholar
- Baron Y, Bargemann T, Harten P, Gutschmidt HJ: Thrombocytopenic thrombotic purpura: severe clinic with no CT, minor MRI, but a SPECT correlate. Eur J Radiol. 1999, 31 (1): 56-62. 10.1016/S0720-048X(98)00088-6.View ArticlePubMedGoogle Scholar
- Limaye S, Cooper J: The right scan at the right time: reversible posterior leukoencephalopathy syndrome mimicking bilateral occipital lobe infarcts. Age Ageing. 2009, 38 (4): 483-484. 10.1093/ageing/afp026.View ArticlePubMedGoogle Scholar
- Peterson PL, Axford JS, Isenberg D: Imaging in CNS lupus. Best practice & research. 2005, 19 (5): 727-739. 10.1016/j.berh.2005.04.001.View ArticleGoogle Scholar
- Moritani T, Shrier DA, Numaguchi Y, Takahashi C, Yano T, Nakai K, et al: Diffusion-weighted echo-planar MR imaging of CNS involvement in systemic lupus erythematosus. Acad Radiol. 2001, 8 (8): 741-753. 10.1016/S1076-6332(03)80581-0.View ArticlePubMedGoogle Scholar
- Ay H, Buonanno FS, Schaefer PW, Le DA, Wang B, Gonzalez RG, et al: Posterior leukoencephalopathy without severe hypertension: utility of diffusion-weighted MRI. Neurology. 1998, 51 (5): 1369-1376. 10.1212/WNL.51.5.1369.View ArticlePubMedGoogle Scholar
- Dilek NO, Gulay K, Emel U, Forta H: Posterior reversible encephalopathy syndrome in systemic lupus erythematosus. Neurol India. 2009, 57 (4): 497-499.View ArticlePubMedGoogle Scholar
- Kinoshita T, Moritani T, Shrier DA, Hiwatashi A, Wang HZ, Numaguchi Y, et al: Diffusion-weighted MR imaging of posterior reversible leukoencephalopathy syndrome: a pictorial essay. Clin Imaging. 2003, 27 (5): 307-315. 10.1016/S0899-7071(02)00592-2.View ArticlePubMedGoogle Scholar
- Covarrubias DJ, Luetmer PH, Campeau NG: Posterior reversible encephalopathy syndrome: prognostic utility of quantitative diffusion-weighted MR images. Ajnr. 2002, 23 (6): 1038-1048.PubMedGoogle Scholar
- Doelken M, Lanz S, Rennert J, Alibek S, Richter G, Doerfler A: Differentiation of cytotoxic and vasogenic edema in a patient with reversible posterior leukoencephalopathy syndrome using diffusion-weighted MRI. Diagn Interv Radiol (Ankara, Turkey). 2007, 13 (3): 125-128.Google Scholar
- The pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1471-2377/12/152/prepub
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.