SN Comprehensive Clinical Medicine

https://doi.org/10.1007/s42399-021-01027-7

MEDICINE

Posterior Reversible Encephalopathy Syndrome with a Distinct

Radiological Pattern Related to Systemic Lupus
Erythematosus—a Case Report and Short Review of Literature
Adriana O. Dulămea 1,2 & Oana Obrișcă 1 & Ioana G. Lupescu 2,3 & Ileana Constantinescu 2,4 & Ioan C. Lupescu 1 &
Gener Ismail 2,5

Accepted: 13 July 2021

# The Author(s), under exclusive licence to Springer Nature Switzerland AG 2021

Abstract
Posterior reversible encephalopathy syndrome (PRES) represents an acute neurological complication, characterized by diverse
symptoms (headache, visual disturbances, altered mental state, seizures, or other focal deficits) that usually relate to uncontrolled
arterial hypertension (HT), eclampsia, sepsis, renal disease, autoimmune disorders, or cytotoxic medication. The accurate
diagnosis relies on radiological features, commonly displaying parieto-occipital vasogenic edema. We report a particular case
of PRES involving the brainstem and capsular-thalamic regions in a patient with systemic lupus erythematosus (SLE). A 25-year-
old female, with a 5-year history of SLE with several manifestations (HT, seizures, lupus nephritis, pericarditis), was admitted for
sudden onset of impaired consciousness and double vision. She was on maintenance immunosuppression, hydroxychloroquine,
and antihypertensive and antiepileptic medication, denying any illicit drug intake or recent infections. The clinical exam revealed
elevated blood pressure, altered mental state, left hemiparesis, bilateral pyramidal signs, ataxia, strabismus, and left facial palsy,
with no meningeal signs or fever. The initial brain CT scan showed diffuse hypodense aspect of the pons, mesencephalon, and
capsular-thalamic regions, confirmed by the MRI exam, displaying extensive hyper-T2-weighted lesions in the same areas,
associating petechial hemorrhages and restricted diffusion. The laboratory work-up excluded infectious encephalitis, vasculitis,
or other metabolic complications, and the favorable clinical-radiological remission confirmed the diagnosis of PRES. We
conducted a literature review regarding PRES in SLE, with special focus on imagistic presentation and major
complications. PRES may complicate the evolution of SLE associated with HT, renal dysfunction, or immunosup-
pression. Neurologists and radiologists should be aware of atypical imagistic patterns and hemorrhagic complications
in PRES, as timely recognition is essential.

Keywords PRES . Systemic lupus erythematosus . Neuroimaging . Immunosuppression

This article is part of the Topical Collection on Medicine

Introduction

* Oana Obrișcă
Posterior reversible encephalopathy syndrome (PRES) repre-
oanaobrisca@gmail.com sents a neurological disorder with acute/subacute onset char-
acterized by various symptoms, including headache, visual
1 disturbances, altered mental state, seizures, and other neuro-
Neurology Clinic, Fundeni Clinical Institute, Sos. Fundeni 258,
022328 Bucharest, Romania logical deficits. It usually occurs in particular clinical condi-
tions, such as arterial hypertension (HT), eclampsia, immuno-
2
University of Medicine and Pharmacy “Carol Davila”, Str. Dionisie
Lupu 37, 020021 Bucharest, Romania suppression, sepsis, renal disease, or autoimmune disorders
3 [1]. In the acute stage, the typical neuroimaging finding con-
Radiology Clinic, Fundeni Clinical Institute, Sos Fundeni 258,
022328 Bucharest, Romania sists of vasogenic edema, predominantly involving the sub-
4 cortical parieto-occipital regions [2, 3].
Center of Immunogenetics and Virology Fundeni, Sos Fundeni 258,
022328 Bucharest, Romania We present a particular case of PRES with a distinct cere-
5 bral imaging, involving the brainstem and capsular-thalamic
Nephrology Clinic, Fundeni Clinical Institute, Sos Fundeni 258,
022328 Bucharest, Romania regions, in a young patient with systemic lupus erythematosus

(SLE) and emphasize the importance of an accurate and time-
ly differential diagnosis.
Case Presentation
A 25-year-old female previously diagnosed with SLE and
related complications, such as malignant HT, seizures, renal
dysfunction, and serositis, was admitted for confusion, double
vision, and slowness in information processing, symptoms
that occurred suddenly on the admission day. The patient de-
nied any recent viral or bacterial infection, vaccination, illicit
drug use, or toxin exposure.
Back in March 2015, at the age of 20, the patient started to
develop arterial hypertension, as she was admitted for one
episode of hypertensive encephalopathy, requiring intensive
care monitoring. At that time, an extensive diagnostic work-
up on secondary causes of HT had been done, but no signif-
icant etiology was established. In the following months, addi-
tional clinical features developed, such as psychiatric manifes-
tations, pericarditis, renal involvement, and Raynaud syn-
drome. The first positive titer of anti-dsDNA antibodies to-
gether with the clinical data clinched the diagnosis of SLE,
consistent with the 2012 SLICC criteria. The kidney biopsy
showed lesions compatible with class VI lupus nephritis and
hypertensive nephropathy. The patient was started on induc-
tion therapy with high-dose regimen of steroids and cyclo-
phosphamide, followed by maintenance therapy with low-
dose steroids, azathioprine, and hydroxychloroquine.
Current treatment included oral prednisolone 16 mg every
other day, azathioprine 50 mg bid, hydroxychloroquine
200 mg bid, fosinopril 10 mg tid, amlodipine 10 mg qd,
pentoxifylline 400 mg qd, sulodexide 250 UI bid, lamotrigine
50 mg bid, fluvoxamine 5 mg qd, and a gastric proton-pump
inhibitor.
At admission, the general examination revealed a somno-
lent patient, with normal body temperature, skin cyanosis,
elevated blood pressure (195/100 mm Hg), sinus rhythm of
100/min, oxygen saturation of 92%, normal pulmonary and
abdominal examination, and preserved diuresis. The neuro-
logical examination showed divergent strabismus of the right
eye, normal brainstem reflexes, left facial palsy, dysarthria,
bilateral limb ataxia, bilateral Babinski sign, and mild left
hemiparesis, with no additional signs of meningeal irritation.
The patient rapidly underwent cerebral CT scan that showed a
diffuse, hypodense aspect of the pons, mesencephalon, and
capsular-thalamic regions (Figure 1). Afterwards, the MRI
exam displayed extensive hyperintense lesions on T2-
weighted sequences, poorly outlined, involving the thalamic,
capsular, and upper brainstem regions and the superior cere-
bellar peduncles, without any restricted diffusion or contrast
enhancement, suggesting vasogenic edema (Figure 2). Acute
petechial hemorrhages with water restriction on DWI and low
SN Compr. Clin. Med.
signal on ADC map with the same anatomical distribution
were also described. The cerebral magnetic resonance angiog-
raphy (MRA) of both the arterial and venous systems
displayed normal blood vessels, without any signs of vaso-
spasm or venous thrombosis.
The laboratory work-up consisted of a serum creatinine
level of 1.3 mg/dl (eGFR of 57 ml/min/1.73m2), mild
hypertriglyceridemia (212 mg/dL), hyperuricemia (11.2 mg/
dL), hypoalbuminemia (2.8 g/dL), and mild leukocytosis (15
000/μL), with slight increase in neutrophils, moderate throm-
bocytopenia (95×103/mm3), increased serum level of fibrino-
gen (562 mg/dL), and C-reactive protein (31 mg/dL, normal
range 0–3 mg/dL). The serum D-dimer level at admission was
in normal range. Cerebrospinal fluid (CSF) examination re-
vealed elevated protein levels (1.5 g/L), normal cell count,
glucose of 62.6 mg/dL, no red blood cells, negative Gram stain,
negative cultures for bacteria, and negative virologic tests, in-
cluding PCR for JC (John Cunningham) virus. Serological tests
for Listeria monocytogenes were negative too.
Shortly after admission, the patient’s condition started to
deteriorate: she became comatose and poorly responsive
(Glasgow Coma Scale of 8 points), developing respiratory
insufficiency, that necessitated intensive care monitoring.
The patient received intravenous dexamethasone 8 mg bid
and unfractionated heparin for thromboembolic protection,
and the antihypertensive medication was carefully adjusted
for proper BP control. Steadily, the general state started to
ameliorate and the focal neurological deficits progressively
remitted. A second cerebral MRI was performed 10 days after
onset, showing a marked improvement of the cerebral edema
and partial remission of the hemorrhagic lesions, remaining
only a few scattered hemosiderin deposits in the left thalamus
and mesencephalon (Figure 3).
The acute symptoms (altered mental state, visual distur-
bances, and neurological deficits), along with the initial cere-
bral imaging, raised the possibility of PRES. The extensive
work-up excluded other possible infectious and metabolic
complications, CNS vasculitis, or other cerebrovascular affec-
tions. Consequently, the favorable clinical remission and
almost-complete radiological resolution pointed out the diag-
nosis of PRES.
Discussion
Posterior reversible encephalopathy syndrome (PRES) is
characterized by reversible vasogenic brain edema, expressed
through various symptoms (headache, seizures, confusion, or
visual disturbances). This clinical-radiological syndrome oc-
curs as a complication of several conditions, such as uncon-
trolled HT, peripartum states, kidney disease, or cytotoxic
treatment [1]. It has been reported in almost all age groups
SN Compr. Clin. Med.

Fig. 1 Initial brain CT scan: hypodense aspect of the upper brainstem and thalamic regions

but is frequently encountered in young/middle-aged adults,
having a female preponderance [3].
Autoimmune disorders are frequently associated with
PRES, as 45% of affected patients have reported a history of
autoimmune diseases, such as SLE, Behcet’s disease, or rheu-
matoid arthritis [4]. Considering that more than 50% of SLE
patients develop neurological symptoms, PRES is still a rare
complication of SLE, occurring in approximately 0.7 to 1.4 %
cases [5–7]. Several risk factors for PRES have been identified
in patients with SLE, such as younger age, high SLEDAI
score ≥ 6 points (SLE disease activity index), uncontrolled
HT, renal dysfunction, lymphopenia, aggressive
immunosuppressive treatments, and dyslipidemia [8–10].
Recently, 2 additional independent risk factors for PRES in
SLE cases have been described: white blood cells > 9×109/L
(OR 2.33 (95% CI: 2.05–2.64)) and heart failure (OR 2.10
(95% CI: 1.18–2.42)) [6]. Most patients seem to develop
PRES within the first year of SLE diagnosis, probably due
to a more active disease or immunosuppression intensification
[7, 11]. SLE might represent the optimal background for
PRES occurrence, as it interferes with the main pathogenic
mechanisms. However, due to its varied clinical manifesta-
tions and, occasionally, insufficient diagnostic evaluation,
symptoms such as seizures might be mistaken as

Fig. 2 Initial cerebral MRI exam: central variant of PRES with edema involving the pons, the midbrain with extension in the capsulo-thalamic regions.
Note also the restricted diffusion areas of the lesions associated with petechial hemorrhagic spots seen in SWI (arrows)

Fig. 3 Second cerebral MRI exam: follow-up MRI evaluation after 1 week. Note the regression of the PRES lesions
neuropsychiatric SLE syndromes. Moreover, it has been im-
plied that PRES should be included in the neuropsychiatric
SLE syndromes for a better clinical recognition and a timelier
effective management [8].
The pathophysiology of PRES is incompletely understood,
and 2 main hypotheses are continuously explored [9]. Firstly,
vascular mechanisms have been implied in PRES develop-
ment, as rapidly developing hypertension exceeds the cerebral
blood flow (CBF) autoregulation mechanisms, causing hyper-
perfusion and further vascular leakage, as a result of the blood-
brain barrier (BBB) dysfunction [1, 2]. The posterior brain
regions might be more susceptible to PRES due to the sparse
sympathetic innervation of the posterior fossa, compared to
anterior regions [10]. However, 15–20% of patients with
PRES are normo- or hypotensive, and among hypertensive
patients, less than 50% have a documented mean BP above
the upper limit of CBF autoregulation (systolic BP > 140–150
mmHg) [4, 12]. Pronounced BP fluctuations, rather than ab-
solute BP increase, might precede the syndrome, assuming
that even patients with sepsis and secondary hypotension
can develop PRES [13]. In SLE cases, renal dysfunction con-
tributes to fluid retention and hypertension, favoring dysreg-
ulation of CBF and development of cerebral edema.
Secondly, the endothelial dysfunction plays a major role in
PRES development, as circulating endogenous (e.g., eclamp-
sia, sepsis) or exogenous toxins (e.g., cytotoxic medication)
SN Compr. Clin. Med.
affect the endothelial integrity, producing vascular leakage
and edema [2, 4, 14, 15]. Endothelial dysfunction is mainly
promoted by proinflammatory cytokines, such as tumor ne-
crosis factor-α (TNF α), interleukin 1 (IL-1), and IL- 6, that
would induce a high expression of adhesion molecules and
VEGF (vascular endothelial growth factor) [16]. VEGF en-
hances the permeability of the BBB, weakening the endothe-
lial intercellular tight junctions [12]. High levels of serum
VEGF have been found in patients with SLE with internal
organ involvement and high disease activity indexes [12].
The damaged BBB might represent a likely mechanism for
PRES in SLE, supported by studies that included the CSF
analysis with albumin quotient, showing increased intrathecal
immunoglobulin synthesis [17]. The frequently encountered
elevated CSF protein levels in PRES have positively correlat-
ed with the severity of edema [14]. However, pleocytosis is
rarely observed (<10% of cases), with the median cell count of
2 cells/μL [15]. In addition, other mechanisms of endothelial
damage have been suggested, such as inflammasome activa-
tion of IL-18 and neutrophil extracellular trap formation, as
well as the role of type I interferon (IFN-I) in depletion of
endothelial progenitor cells (high levels of IFN-1 have been
documented in SLE) [18]. Dyslipidemia and lymphopenia,
frequently seen in SLE patients, could further promote the
endothelial abnormalities [19].
SN Compr. Clin. Med.
Immunosuppressive medication used for controlling the
SLE activity might also be a significant factor in PRES occur-
rence. In a reviewed series of PRES episodes in SLE patients,
98% of them were receiving corticosteroids, 40% were on
cyclophosphamide, and 3.9% on cyclosporine [20]. There
are few case reports about the association of azathioprine with
PRES, where neurological symptoms have developed shortly
after azathioprine initiation, unlike the case of our patient with
long-term azathioprine and corticosteroid treatment [21, 22,
23].
Since PRES has no specific biomarker or test, the diagnosis
relies mostly on clinical symptoms, correlated with cerebral
imaging, preferably MRI due to its higher accuracy in exclud-
ing other pathologies [1]. The clinical picture of PRES in SLE
patients is similar to other cases of PRES with various triggers,
consisting of seizures, as the most common manifestation,
followed by headache, visual disturbances, and altered mental
state [7, 24]. Rarely, the initial symptoms represent status
epilepticus or a comatose state [6]. Focal neurological signs
have been encountered in 5–15% of patients with PRES [3].
The majority of the symptoms are reversible, but severe com-
plications might occur, such as status epilepticus, cerebral
ischemia, intracerebral hemorrhage, or acute intracranial hy-
pertension, requiring intensive care monitoring [25].
PRES is classically characterized by bilateral, subcortical
vasogenic edema, involving mostly the parieto-occipital re-
gions [22]. CT examination frequently represents the first im-
agistic evaluation, displaying white matter hypoattenuation,
and is usually followed by MRI studies that have increased
sensitivity and contribute to a more accurate differential diag-
nosis (e.g., cerebral infarction, demyelinating processes, infec-
tious etiologies, vasculitis, metabolic disturbances, or progres-
sive multifocal leukoencephalitis) [26]. Among PRES
mimics, reversible cerebral vasoconstriction syndrome
(RCVS) is worthy of note, since it manifests through similar
symptoms (thunder-clap headache, seizures, stroke) but typi-
cally occurs during the postpartum period or after exposure to
adrenergic or serotoninergic medications [27]. The imagistic
particularities of this syndrome are non-aneurysmal subarach-
noid hemorrhage and multifocal narrowing of the cerebral
arteries, best observed in angiographic studies. Nevertheless,
PRES and RCVS might occur simultaneously, so attentive
imagistic exam contributes to the correct diagnosis [23].
Four different radiological patterns in PRES have been
outlined so far: (1) parieto-occipital pattern, encountered in
the majority of cases (50–55%), (2) superior frontal sulcus
pattern (21–27%), (3) holo-hemispheric watershed pattern
(23–29%), and (4) central pattern (13%), characterized by
edema of the deep cerebral structures (deep white matter, basal
ganglia, and brainstem) [22, 24, 28]. The parieto-occipital
vasogenic edema is the most frequently encountered pattern
in PRES occurring in SLE patients, but in a few cases, occip-
ital involvement might be missing (Table 1) [7, 10, 27].
Asymmetric or unilateral involvement had been described,
together with atypical imaging findings, such as contrast en-
hancement, restricted diffusion, or hemorrhage [34]. Pediatric
patients with PRES, frequently determined by renal diseases,
tend to associate more atypical imaging features, including
frontal lobe involvement [35]. Prior to the development of
typical parieto-occipital edema, one might encounter early
signs of PRES, such as minor sulcal FLAIR hyperintensities
and leptomeningeal-enhancement on postcontrast T1-
weighted images [36]. A recent large sample study showed
that the neurological symptoms of patients with PRES with
atypical imagistic patterns did not entirely correspond to the
brain lesion locations (brainstem lesions had been seen in
20.7% of patients, and still most of them had no spe-
cific symptomatic correlations) [37]. Moreover, 23% of
patients developed cytotoxic edema, and residual infarc-
tion was seen in only 2 cases, confirming it as a rare
complication of PRES. Over a third of the patients
displayed contrast-enhancing lesions and obstructive hy-
drocephalus developed in few cases, mainly due to sig-
nificant infratentorial edema [37].
Hemorrhagic complications might occur in approximately
15–25% of PRES cases under three distinct forms: (1) large,
focal intraparenchymal hematoma, (2) subarachnoid hemor-
rhage, or (3) cerebral microbleeds (CMB) [38–40]. Recent
studies have reported higher prevalence of cerebral hemor-
rhage in PRES (26–64%), by using SWI-sequence (suscepti-
bility-weighted imaging), as it is the most sensitive method for
detecting CMB [41, 42]. The direct effect of CMB on prog-
nosis remains incompletely understood, since they tend to
persist on follow-up studies, implying possible future compli-
cations [41]. On the other hand, prior CMB might be involved
in PRES development, as it could be inferred from previous
reports of PRES secondary to cerebral amyloid angiopathy
inflammation [43].
Recently, more advanced imaging techniques have been
described as complementary tools used in more challenging
cases, consisting of CT/MR perfusion studies, MR spectros-
copy (MRS), or nuclear medicine techniques (SPECT) [26,
44]. Using MR/CT perfusion exams, mostly hyperperfusion
has been encountered in cerebral regions affected by PRES,
but hypoperfusion patterns have also been reported [45]. MRS
or PET studies are useful in differentiating PRES from other
pathologies, such as tumors, encephalitis, or demyelination,
especially when asymmetric or unilateral radiological presen-
tations occur [44]. The follow-up imaging usually shows com-
plete or near-complete resolution of cerebral abnormalities in
up to 70% of cases, as it has been illustrated in our patient too
[40]. The most influential prognostic factors are reversibility
of lesions and cerebral hemorrhagic complications [46, 47]. In
addition, restricted diffusion suggesting cytotoxic edema (de-
creased ADC values on MRI) and hypoperfusion can be en-
countered in 15–30% of cases, contributing to irreversible
Table 1 Imagistic findings in SLE patients with PRES

Author No. of Vasogenic edema Asymmetrical/ ICH Restricted Remarks

pts. unilateral diffusion/infarction
Occipital Parietal Frontal Temporal Cerebellum Central
region region lobe lobe pattern

Baizabal-Carvallo et al 22 81% 59% 36.3% 40.9% 54.5% 9–18% NR 9% 13.3% The imagistic patterns supported the diffuse nature
(2008) [17] of PRES, with a posterior-anterior gradient.
Cortical involvement in 95.5% of patients
underlined the high frequency of seizures in this
cohort
Barber et al (2011) [29] 7 85.7% 71.4% 42.8% 14.2% 14.2% 14.2% 14.2% 42.8% NR The hemorrhagic complications varied from
bilateral hematomas to discrete cortical
microhemorrhages
Liu et al (2012) [30] 10 100% 80% 66.7% 50% 20% 10% 10% 10% 40% Two patients displayed normal initial MRI scans
despite suggestive neuropsychiatric symptoms
and only the follow-up MRI showed posterior
vasogenic edema after 2 weeks
Shaharir et al (2013) [31] 87 NR NR NR NR 22.9% 11.4% 5.7% 8.7% NR Intracranial hemorrhage and brainstem
involvement are two important predictors of
poor outcome in PRES
Lai et al (2013) [32] 23a) 100% 76.9% 53.8% 65.4% 34.6% NR NR 15.4% NR Severe hypoalbuminemia and thrombocytopenia
are risk factors for PRES-related ICH
Jung et al (2013) [33] 15 93.3% 80% 66.7% 60% 26.7% 13.3% NR NR NR After brain MRIs’ reviews, 4 patients were
suspected to have cerebral vasculitis
Merayo-Chalico et al 48 84% NR NR NR NR NR NR NR NR Control MRI: cerebral lesions diminished in size
(2016) [19] or completely resolved in 84.6% of patients
Budhoo et al (2015) [7] 10 90% 90% 50% 20% 30% 20% NR 10% NR Main trigger for PRES in SLE in this
South-African cohort was disease activity

Central pattern-edema of the deep cerebral structures (deep white matter, basal ganglia or brainstem); Pts patients, NR not reported, PRES posterior reversible encephalopathy syndrome, SLE systemic lupus
erythematosus, ICH intracerebral hemorrhage
a)
23 patients included in the study with 26 episodes of PRES
SN Compr. Clin. Med.
SN Compr. Clin. Med.
cerebral lesions and incomplete recovery or unfavorable out-
come [38, 48].
Above all, PRES has a good prognosis, with a complete
clinical recovery within 1 week in 75–90% of cases [19, 49].
Death occurs in approximately 8 to 17% of affected patients,
mostly depending on the underlying disease [19]. Siebert et al.
identified several factors that were significantly more frequent
in patients who died in hospital, such as altered mental state,
subarachnoid hemorrhage, higher levels of C-reactive protein,
and altered coagulation [38]. In patients with severe PRES,
incomplete recoveries might easily be encountered, as 44% of
patients had some sort of functional deficit at 90 days after the
event in a follow-up study [50]. Moreover, PRES recurrence
has been described in 5–10% of patients, particularly related
to uncontrolled hypertension [46]. In a recent large retrospec-
tive cohort of PRES patients, end-stage renal disease, atrial
fibrillation, and malignancy appeared to be linked with a very
high risk of mortality [51]. Regarding PRES secondary to
SLE, patients have great chances to completely recover in
the first 72 h, as has been described in 93.7 % of the patients
from a large case-control study [19]. However, other group
reported a complete recovery within 1 week in 90% of cases
[6].
A successful management of PRES starts with its prompt
recognition, based on the clinical and radiological picture,
followed by removal of the underlying cause (e.g., cessation
of the toxic medication), adequate BP control, and seizure
control [2, 4, 52]. In SLE patients, there are intricate patho-
genic factors that concur to PRES development, such as un-
controlled hypertension, high doses of corticosteroids, or im-
munosuppressive drugs, making its management even more
difficult. Nevertheless, effective BP control is frequently nec-
essary, together with prompt withdrawal of the immunosup-
pressive agents, whenever it is the case [1]. However, PRES
has been associated with active SLE (SLEDAI score ≥6,
SLEDAI-N score >12), and that usually requires continuous
and increased immunosuppressive therapy [6, 19].
Consequently, immunosuppression should not be
discontinued or reduced in patients with SLE and PRES, but
instead it should be escalated for a better control of active SLE
[6].
Coming back to our case, arterial hypertension and a com-
plicated autoimmune disease (SLE) were the main triggers for
PRES development. Our patient presented several risk factors
for PRES, such as young age, renal dysfunction, arterial hy-
pertension, and dyslipidemia. The patient was on chronic im-
munosuppressive medication, with good tolerance, and no
recent change in her treatment had been done, making it less
probable for the immunosuppressive treatment to cause the
PRES episode. The clinical remission was impressive, but
our patient needed a longer time for complete recovery (al-
most 2 weeks).
Conclusions
This case report illustrates a particular PRES episode, occur-
ring as a rare complication of SLE and having distinct imaging
features, such as vasogenic edema with a central pattern and
acute petechial hemorrhages with the same anatomical distri-
bution. Timely recognition of this neuro-radiological syn-
drome and its imaging particularities is essential for adequate
therapeutic measures.
Abbreviations ADC, apparent diffusion coefficient; BBB, blood-brain
barrier; BP, blood pressure; CBF, cerebral blood flow; CMB, cerebral
microbleeds; CNS, central nervous system; CSF, cerebrospinal fluid;
CT-scan, computed tomography scan; HT, arterial hypertension; IL, in-
terleukin; MRA, magnetic resonance angiography; MRI, magnetic reso-
nance imaging; MRS, magnetic resonance spectroscopy; PRES, posterior
reversible encephalopathy syndrome; RCVS, reversible cerebral vasocon-
striction syndrome; SLE, systemic lupus erythematous; SLEDAI, system-
ic lupus erythematous disease activity index; SWI, susceptibility weighted
imaging; TNF, tumor necrosis factor; VEGF, vascular endothelial growth
factor
Author Contribution Adriana O. Dulamea together with Gener Ismail
have successfully managed the patient during her entire disease history.
Ioana G. Lupescu was responsible for the entire radiological exams.
Ileana Constantinescu contributed with the extensive laboratory work-
up. Oana Obrisca collected the clinical data and was in charge with the
detailed literature research and with the first draft of the article. All the
authors revised the materials and contributed to the final manuscript.
Data Availability Patient’s clinical information and medical history were
obtained from the Nephrology Department - “Fundeni Clinical Institute,”
Bucharest, Romania. The scientific information and recent data were
gathered from articles and publications after a thorough search in the main
online databases (e.g., PubMed).
Declarations
Ethics Approval Not applicable.
Consent to Participate Not applicable.
Consent for Publication Written informed consent was obtained from
the patient, so that all her medical data could be used for scientific pur-
poses, including publication.
Competing Interests The authors declare no competing interests.
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