Cme Reviewarticle

CHIEF EDITORS NOTE: This article is part of a series of continuing education activities in this Journal through which a total
of 36 AMA PRA Category 1 Creditscan be earned in 2014. Instructions for how CME credits can be earned appear on the
last page of the Table of Contents.
Long-term Consequences of the Posterior
Reversible Encephalopathy Syndrome in
Eclampsia and Preeclampsia: A Review of
the Obstetric and Nonobstetric Literature
Ineke R. Postma, BSc,* Sjoerdtje Slager, BSc, Hubertus P.H. Kremer, MD, PhD,
Jan Cees de Groot, MD, PhD, and Gerda G. Zeeman, MD, PhDk
*Medical/PhD Student, and Medical Student, Department of Obstetrics and Gynaecology, Neurologist, Department of
Neurology, Radiologist, Department of Radiology, and kObstetrician, Department of Obstetrics and Gynaecology, University
Medical Center Groningen, University of Groningen, Groningen, The Netherlands
This review summarizes the long-term consequences of the posterior reversible encephalopathy syn-
drome (PRES) that have been described in the obstetric literature (eclampsia and preeclampsia) and
compares these with data from the nonobstetric literature. Preeclampsia is characterized by new-onset
hypertensionandproteinuria after the 20th week of pregnancy. Neurological symptoms includeheadache;
visual deficits; confusion; seizures; and, in the most severe cases, intracranial hemorrhage. Eclampsia is
an acute cerebral complication of preeclampsia, defined as the occurrence of tonic-clonic seizures in
pregnant or recently postpartum women. With severe preeclampsia, in conjunction with neurological
symptoms, or eclampsia, neuroimaging changes consistent with PRES can be seen. Posterior reversible
encephalopathy syndrome is a specific clinicoradiological syndrome presenting with headaches, visual
impairment, seizures, and altered mental status. Characteristic neuroimaging features are consistent with
cerebral edema predominantly in the parietal and occipital lobes. In addition to preeclampsia/eclampsia,
PRES has been associated with various conditions in the nonobstetric population, that is, severe hyper-
tension, transplantation, or autoimmune disease, in combination with immunosuppressive therapy or
high-dose chemotherapy for various malignant conditions. Long-term sequelae of both preeclampsia/
eclampsia and other PRES-related conditions are poorly described. After eclampsia or preeclampsia,
nonspecific white matter lesions may be found on magnetic resonance imaging, which may or may not
be related to the PRES episode. Previously (pre)eclamptic women report cognitive failures; however, no
neurocognitive impairment has been shown so far. Various nonobstetric PRES-related conditions have
been described with long-termneuroimaging abnormalities as well as cognitive problems, epilepsy, or vi-
sual impairment. Although no firm conclusions can be drawn because of the heterogeneity of reported
cases, some general comments can be made. Because most persistent long-term problems are present
in the nonobstetric population, the main determinant for these long-termproblems may be the underlying
condition that gave rise to the PRES episode. In addition, most reports suggest that late diagnosis or in-
adequate therapy may contribute, emphasizing the need for early recognition, adequate treatment,
follow-up, and support.
Target Audience: Obstetricians and gynecologists, neurologists, radiologists, ophthalmologists, psychologists
LearningObjectives: After completingthis CMEactivity, thereader shouldbeabletoidentify theclinicoradiological
syndrome and pathophysiology of PRES in preeclampsia/eclampsia, evaluate long-term consequences and
complaints in formerly preeclamptic and eclamptic women, and determine the need for early magnetic resonance im-
aging diagnosis of PRES.
All authors and staff in a position to control the content of this CME
activity and their spouses/life partners (if any) have disclosed that they
have no financial relationships with, or financial interests in, any com-
mercial organizations pertaining to this educational activity.
Correspondence requests to: Ineke R. Postma, BSc, Department of
Obstetrics and Gynaecology, University Medical Center Groningen,
Hanzeplein 1, CMC IV, CB21, 9700 RB Groningen, The Netherlands.
E-mail: i.r.postma@umcg.nl.
www.obgynsurvey.com | 287
Volume 69, Number 5
OBSTETRICAL AND GYNECOLOGICAL SURVEY
Copyright 2014
by Lippincott Williams & Wilkins
CME REVIEWARTICLE
14
Copyright 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Background and Aims
Preeclampsia is a hypertensive, multisystem disorder
of pregnancy and is a leading cause of maternal and
fetal/neonatal morbidity and mortality. It is defined as
new-onset hypertension combined with proteinuria after
the 20th week of pregnancy. The central nervous system
can be involved during the course of preeclampsia in the
form of hyperreflexia; headaches; visual disturbances;
mental status changes; eclampsia; and, in the most severe
cases, intracranial hemorrhage. Eclampsia is an acute ce-
rebral complication of preeclampsia, defined as the oc-
currence of tonic-clonic seizures in pregnant or recently
postpartum women. Eclampsia is responsible for signifi-
cant maternal and neonatal morbidity and mortality
worldwide. The overall worldwide estimate of the inci-
dence of preeclampsia and eclampsia is 4.6% and 1.4%
of deliveries, respectively, with an estimated 15.6% and
4%in developing countries and 3.3%and 0.1%in devel-
oped countries.
1,2
Eclampsia incidence has significantly
decreased since the introduction of management guide-
lines for eclampsia and preeclampsia, including the use
of magnesium sulfate for seizure prophylaxis. The under-
lying pathophysiology of preeclampsia includes hyper-
tension and generalized endothelial cell dysfunction.
Eclampsia is considered to be a form of the posterior
reversible encephalopathy syndrome (PRES).
3,4
In
some women with severe preeclampsia, particularly those
with neurological symptoms such as severe headache or
visual disturbances, PRES may also occur.
3,5
Posterior re-
versible encephalopathy syndrome was coined revers-
ible because, in the first series of 15 patients (among
whom 3 women had eclampsia), described by Hinchey
et al
6
in the mid-1990s, both the clinical and neuroimaging
abnormalities seemed to resolve after normalization of the
blood pressure and removal of the underlying cause. How-
ever, since this original publication, several reports have
been published in which long-term neuroimaging abnor-
malities and/or neurological and cognitive problems seem
to persist. For instance, subjective cognitive dysfunction
and impaired vision-related quality of life have been
reported in the years after preeclampsia.
79
Whether these
symptoms are related to the PRES episode is unknown.
Unfortunately, systematic follow-up of PRES patients is
largely lacking, both in obstetric and nonobstetric cohorts.
We aimed to reviewthe literature for existing information
on possible long-term sequelae of PRES in preeclampsia
and eclampsia and to compare this with follow-up studies
in nonobstetric patients with conditions related to PRES.
Literature Search Strategy
The search strategy included a MEDLINE search
up to June 2013 limited to publications in the English
language and to reports of human patients. The fol-
lowing Medical Subject Headings terms were used:
preeclampsia, eclampsia, posterior leukoencephalop-
athy syndrome, hypertensive encephalopathy, MRI,
neuroimaging, cognition disorders, quality of life, epi-
lepsy, and vision disorders. In addition, the following
PubMed terms were reviewed: posterior reversible en-
cephalopathy syndrome, PRES, RPLS, leukoenceph-
alopathy, preeclampsia, eclampsia, long-term, white
matter lesions, and white matter hyperintensities.
Abstracts were reviewed for suitability by the first 2
authors; follow-up of the described subjects had to be
available for clinical characteristics, neuroimaging, or
both. The bibliographies of the available articles were
subsequently cross-referenced. The literature retrieved
consisted mainly of isolated case reports and some
small case series. In total, 1695 articles were identified,
of which 55 were deemed suitable (ie, described
follow-up of clinical characteristics, neuroimaging, or
both; were written in English; and involved human
patients) and included in this review.
PRES: Definition and Diagnosis
Posterior reversible encephalopathy syndrome, also
known as the reversible posterior leukoencephalopathy
syndrome (RPLS), reversible posterior cerebral edema
syndrome, or reversible occipitoparietal encephalopa-
thy, is a condition that has been associated not only
with preeclampsia and eclampsia but also with numer-
ous systemic conditions in nonobstetric patients of all
ages. As shown in Table 1, it has been described in
conjunction with malignant hypertension, sepsis, allo-
geneic bone marrow or stem cell transplantation, solid
organ transplantation, or autoimmune disease, in com-
bination with immunosuppressive therapy and/or high-
dose chemotherapy for various malignant or chronic
autoimmune conditions. Several other conditions have
anecdotally been associated with PRES.
1013
Posterior
reversible encephalopathy syndrome is a neurotoxic
and neurometabolic condition characterized by a ty-
pical clinicoradiological syndrome.
6
(Holocephalic)
headaches; visual impairment such as blurred vision,
visual field defects, or blindness; focal neurological
deficits; seizures; altered mental status; and, in some
patients, coma are the symptoms and signs typically
observed.
10,11,1416
Computed tomography (CT) fea-
tures of PRES consist of either hypodense areas con-
sistent with edema or no specific abnormalities.
6
Magnetic resonance imaging (MRI) shows a uniform
and characteristic pattern of T2 and fluid-attenuated
inversion recovery (FLAIR) hyperintense areas consis-
tent with edema, which predominantly affect the white
288 Obstetrical and Gynecological Survey
and gray matter of the parietal and occipital lobes.
17
Diffusion-weighted imaging (DWI) and apparent dif-
fusion coefficient (ADC) mapping are the techniques
of choice to distinguish between vasogenic and cyto-
toxic cerebral edema. In PRES, cerebral edema is pri-
marily thought to be of vasogenic nature. Water
mobility is increased, as demonstrated by normal, de-
creased but sometimes also increased DWI signal in-
tensity of the hyperintense T2 regions, whereas ADC
mapping shows increased signal intensity. Vasogenic
edema (due to temporary insufficiency of the blood-
brain barrier for water diffusion) is generally revers-
ible, whereas cytotoxic edema implies local infarction.
In cytotoxic edema, there is decreased water mobility
consistent with a hyperintense DWI signal, whereas
ADC mapping (indicating whether diffusion is re-
stricted, unchanged, or enhanced in the area of the hy-
perintense DWI signal) is decreased,
1820
showing
hypointense on the ADC image. In severe cases, it
has been suggested that vasogenic interstitial edema
can progress to the extent that it may cause decreased
regional perfusion to ischemic levels resulting in cyto-
toxic edema.
18
Although the posterior regions of the
brain seem most commonly affected, the frontal lobes,
the inferior temporal-occipital junction, the cerebel-
lum, the basal ganglia, the brain stem, and deep white
matter may be involved as well.
15,21,22
This distribu-
tion of cerebral edema may be related to local levels
of perfusion in vascular watershed areas or regions with
mainly end-arterial vascular supply. Perfusion scanning
using
99m
Tc-hexamethylpropyleneamine oxime single
photon emission computed tomography has rarely
been used in PRES research, and results are not con-
clusive; both hyperperfusion and hypoperfusion have
been described.
23,24
PRES: Prevalence and Pathophysiology
The incidence of PRES has not been established to
date. Hinchey et al
6
were the first to describe 15
patients, with various comorbid conditions, including
3 women with eclampsia. Nonobstetric conditions in-
cluded renal insufficiency, malignant hypertension,
or conditions for which immunosuppressive therapy
had been initiated. It is generally thought that the
common denominator for the development of PRES
is the presence of some degree of hypertension in
combination with cerebrovascular endothelial dys-
function, as can be seen in women with preeclamp-
sia.
21
The cause of PRES in nonobstetric patients
who are treated with immunosuppressive or chemo-
therapy is not completely understood. Hypertension
(sometimes associated with corticosteroid treatment)
in combination with low magnesium-calcium ratio
and brain microvascular physiological changes in-
duced by the therapy are thought to play a role, a
mechanism that is, in some aspects, similar to pre-
eclampsia.
6,24
Acute severe hypertension may play
a role in PRES, but in 20% to 30% of women with
eclampsia, blood pressure values have been reported
to be within the usual cerebral autoregulatory range.
25
Although the exact pathophysiological mechanism for
the development of cerebral edema in PRES remains
unclear, impaired cerebrovascular autoregulatory ca-
pacity is likely to be involved. The cerebrovascular
endothelium plays an important role maintaining auto-
regulation, acting through vasomotor effectors that con-
trol cerebrovascular resistance in vascular wall lining
pericytes.
26,27
Furthermore, the cerebrovascular endo-
thelium also functions as the blood-brain barrier, which
prevents bulk flow of water and solutes by tight
junctions between the endothelial cells.
26
Posterior
reversible encephalopathy syndrome is thought to de-
velop when an increase in blood pressure, in conjunction
with endothelial cell dysfunction, exceeds the upper
limit of cerebrovascular autoregulation and results in
forced vasodilatation of the cerebral resistance vessels.
Subsequent hyperperfusion; capillary bed injury; and,
eventually, breakthrough of the blood-brain barrier
with resulting vasogenic edema are thought to be its
pathophysiological hallmarks.
21
TABLE 1
Medications and Conditions Associated With PRES
Medication Underlying Conditions
Asparaginase Preeclampsia/eclampsia
Bevacizumab Malignant hypertension
Carboplatin Autoimmune diseases
Cyclophosphamide Transplant recipients
Cyclosporin Sepsis
Fluorouracil Kidney disease
Gemcitabin Excessive licorice consumption
Hydroxycarbamide Various malignancies
Hydroxychloroquine
Infliximab
Methotrexate
Mycophenolate mofetil
Paclitaxel
Rituximab
Sirolimus
Sorafenib
Tacrolimus
Thalidomide
Vincristine
Stroescu et al,
10
Burnett et al,
11
Staykov et al,
12
Bartynski et al.
13
289 Review of Long-term Consequences of PRES CME Review Article
PRES AND LONG-TERM
NEUROIMAGING FEATURES
The neuroimaging studies reporting short- or long-
term follow-up in preeclampsia and eclampsia are
summarized in Table 2 (upper part). Liman et al
28
de-
scribe focal gliosis in 40% of women who had PRES
associated with preeclampsia-eclampsia, after a mean
of 9 days (minimum2 days, maximum38 days). Zeeman
et al
18
found that 19%of eclamptic women had imaging
abnormalities such as white matter infarction and areas
of gliosis after 6 to 9 weeks. Our group
29,30
found that,
on long-term follow-up (mean of 7 years), the preva-
lence of cerebral white matter lesions (WMLs) in both
formerly eclamptic (41%) and preterm preeclamptic
women (37%) was significantly higher compared with
age-matched women who had had a normotensive preg-
nancy (17%21%). These atypical lesions were predom-
inantly found in the frontal lobes and, less often, in the
parietal, insular, and temporal lobes, which is not the typ-
ical distribution pattern of PRES.
31
Although the patho-
genesis of these WMLs remains to be elucidated, an
increased propensity for cerebrovascular disease in
women with a history of preeclampsia may be a factor
in the development of these WMLs.
Table 2 (lower part) summarizes studies reporting
short- or long-term follow-up in a variety of primar-
ily nonobstetric conditions underlying the develop-
ment of PRES.
11,19,22,3243
These studies reported
anywhere between 6 and 151 patients with a large va-
riety of PRES-associated underlying conditions and
age ranges. Some of these studies also included
eclamptic and preeclamptic women
11,22,32,35,36,38,39,42
;
only half of them compared outcome variables based
on the underlying cause of PRES.
22,32,35,38
All re-
ports describe imaging abnormalities, frequently
consisting of nonspecific WMLs and infarction, in
a wide frequency range (15%70%) of PRES pa-
tients.
11,19,22,3236,3843
Furthermore, a variety of
clinical symptoms are described, such as neurolog-
ical deficits, visual abnormalities, cognitive impair-
ment, and even death. These clinical symptoms might
or might not be directly related to the PRES epi-
sode and/or the underlying condition. The time span
between initial and follow-up MRI investigations dif-
fered widely, between 24 days and 6 years in individ-
ual series.
Liman et al
28
specifically studied the clinicoradio-
logical differences between PRES in preeclampsia/
eclampsia on the one hand and PRES in nonobstetric
conditions (immunosuppression, infection/sepsis, au-
toimmune disorders, and chemotherapy) on the other.
Women with preeclampsia/eclampsia had less severe
edema compared with the other predisposing conditions,
had less often radiological evidence for cytotoxic edema,
hemorrhage, and contrast enhancement; and had less
frequent residual structural lesions on follow-up imag-
ing (40% had gliosis after preeclampsia/eclampsia,
whereas infarction, hemorrhagic residua, cerebral atro-
phy, and laminar necrosis were more prominent in
nonobstetric conditions). Hefzy et al
38
found that patients
with immunosuppressive therapyrelated PRES, espe-
cially associated with allogeneic bone marrowtransplan-
tation, are more likely to have accompanying intracranial
hemorrhage as compared with PRES related to eclamp-
sia/preeclampsia. The reason for the high rate of PRES-
related hemorrhage in this group is not clear. The authors
speculate that allogeneic bone marrow transplantation
induces a complex clinical state, in which graft-versus-
host effects, veno-occlusive disease, thrombotic micro-
angiopathy, and opportunistic infection synergize with
high-dose immunosuppressive drugs. The combined
effects may lead to increased cerebrovascular insta-
bility and an increased risk for hemorrhage.
PRES AND LONG-TERM
COGNITIVE DEFICITS
Women with eclampsia/preeclampsia report more
long-term (mean of 7 years) subjective cognitive diffi-
culties related to memory and concentration compared
with women who had uncomplicated pregnancies, us-
ing the Cognitive Failures Questionnaire.
7,8
In con-
junction with the WML seen on neuroimaging years
later, it has been hypothesized that subtle neuro-
cognitive problems may exist when measured by
neurocognitive examination. Stroescu et al
10
describe
a 30-year-old woman with late-onset postpartum pre-
eclampsia who underwent both imaging and follow-up
neuropsychological examination. In the acute phase,
she had hyperintense abnormalities on FLAIR MRI bi-
laterally in the occipital and posterior parietal lobes. She
was referred for neurocognitive examination 11 months
later and showed decreased working memory and visual
attention, spatial perception deficits, decreased motor
speed, visuospatial memory, and executive dysfunction.
At follow-up MRI 19 months later, she demonstrated bi-
lateral parietal lobe infarcts. Andersgaard et al
44
inter-
viewed 123 formerly eclamptic women 6 to 24 months
postpartum by means of a structured telephone inter-
view. They found that 2 patients had hemiparesis and
dysarthria, 11%had visual disturbances, 22% had con-
centration and memory problems, 18% reported fre-
quent headaches, and 10% had vertigo or balance
problems. Although such women may report subjective
cognitive dysfunction, recent data do not demonstrate
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3
4
4
5
y
,
9
/
1
3
9
(
2
6
%
)
2
7
d
1
.
5
T
,
T
1
/
T
2
,
F
L
A
I
R
,
D
W
I
5
5
%
H
i
g
h
D
W
I
i
n
t
e
n
s
i
t
y
i
n
6
(
2
7
%
)
i
n
d
i
c
a
t
i
v
e
o
f
c
y
t
o
t
o
x
i
c
e
d
e
m
a
;
2
p
r
o
g
r
e
s
s
e
d
t
o
i
n
f
a
r
c
t
i
o
n
,
3
h
a
d
r
e
s
i
d
u
a
l
l
e
s
i
o
n
s
,
g
l
i
o
s
i
s
,
s
u
b
a
c
u
t
e
i
n
f
a
r
c
t
i
o
n
D
e
a
t
h
(
n
=
5
)
E
c
l
a
m
p
s
i
a
2
0
%
N
o
n
e
N
o
t
d
e
s
c
r
i
b
e
d
(
C
o
n
t
i
n
u
e
d
o
n
n
e
x
t
p
a
g
e
)
T
A
B
L
E
2
.
(
C
o
n
t
i
n
u
e
d
)
P
R
E
S
-
A
s
s
o
c
i
a
t
e
d
C
o
n
d
i
t
i
o
n
P
R
E
S
C
a
s
e
s
,
N
M
e
a
n
/
M
e
d
i
a
n
A
g
e
(
S
D
/
I
Q
R
)
,
N
m
/
f
N
(
%
)
W
i
t
h
F
o
l
l
o
w
-
u
p
M
e
a
n
/
M
e
d
i
a
n
F
o
l
l
o
w
-
u
p
T
i
m
e
(
S
D
/
I
Q
R
)
M
R
I
S
e
q
u
e
n
c
e
s
%
o
f
N
W
i
t
h
I
m
a
g
i
n
g
A
b
n
o
r
m
a
l
i
t
i
e
s
a
t
F
o
l
l
o
w
-
u
p
S
p
e
c
i
f
i
c
F
o
l
l
o
w
-
u
p
I
m
a
g
i
n
g
A
p
p
e
a
r
a
n
c
e
C
l
i
n
i
c
a
l
S
y
m
p
t
o
m
s
a
t
F
o
l
l
o
w
-
u
p
P
a
n
d
e
2
0
0
6
E
c
l
a
m
p
s
i
a
,
H
E
,
I
M
,
T
T
P
,
R
F
5
2
3
1
y
,
1
8
/
3
4
5
2
(
1
0
0
%
)
4
6
(
1
4
2
7
0
)
d
0
.
5
/
1
.
5
T
,
T
1
/
T
2
,
F
L
A
I
R
,
D
W
I
E
c
l
a
m
p
s
i
a
0
%
8
%
2
4
%
s
u
b
c
o
r
t
i
c
a
l
w
h
i
t
e
m
a
t
t
e
r
N
o
t
d
e
s
c
r
i
b
e
d
H
y
p
e
r
t
e
n
s
i
o
n
3
6
%
5
6
%
b
r
a
i
n
s
t
e
m
C
h
e
m
o
t
h
e
r
a
p
y
4
3
%
5
3
%
d
e
e
p
w
h
i
t
e
m
a
t
t
e
r
R
e
n
a
l
f
a
i
l
u
r
e
6
0
%
4
0
%
t
h
a
l
a
m
u
s
E
c
l
a
m
p
s
i
a
1
3
0
%
N
o
n
e
N
o
t
d
e
s
c
r
i
b
e
d
L
e
e
2
0
0
8
E
c
l
a
m
p
s
i
a
,
H
E
,
I
M
3
6
4
3
(
1
7
)
y
,
1
6
/
2
0
3
5
(
9
2
%
)
1
3
8
,
8
0
%
<
6
m
o
N
o
t
d
e
s
c
r
i
b
e
d
3
4
%
S
m
a
l
l
r
e
s
i
d
u
a
l
i
n
f
a
r
c
t
s
i
n
~
2
5
%
N
o
r
e
c
u
r
r
e
n
t
s
e
i
z
u
r
e
s
E
c
l
a
m
p
s
i
a
4
N
o
t
d
e
s
c
r
i
b
e
d
N
o
t
d
e
s
c
r
i
b
e
d
N
o
t
d
e
s
c
r
i
b
e
d
H
e
f
z
y
2
0
0
9
E
c
l
a
m
p
s
i
a
,
H
E
,
I
M
,
C
T
,
A
D
,
s
e
p
s
i
s
1
5
1
w
i
t
h
P
R
E
S
,
2
3
w
i
t
h
I
C
H
4
6
y
,
7
/
1
6
N
o
t
d
e
s
c
r
i
b
e
d
N
o
t
d
e
s
c
r
i
b
e
d
1
.
5
T
,
T
1
/
T
2
1
5
.
2
%
(
i
m
m
u
n
e
s
u
p
p
r
e
s
s
i
o
n
2
2
%
,
e
c
l
a
m
p
s
i
a
6
%
)
I
n
t
r
a
c
r
a
n
i
a
l
h
e
m
o
r
r
h
a
g
e
(
I
C
H
)
,
2
h
a
d
d
e
l
a
y
e
d
h
e
m
a
t
o
m
a
H
e
m
i
p
a
r
e
s
i
s
/
h
e
m
i
a
n
o
p
s
i
a
(
n
=
1
)
,
d
e
a
t
h
(
n
=
6
)
E
c
l
a
m
p
s
i
a
1
8
6
%
I
n
t
r
a
c
r
a
n
i
a
l
h
e
m
o
r
r
h
a
g
e
(
I
C
H
)
N
o
t
d
e
s
c
r
i
b
e
d
B
u
r
n
e
t
t
2
0
1
0
P
r
e
e
c
l
a
m
p
s
i
a
/
e
c
l
a
m
p
s
i
a
,
H
E
,
C
T
,
I
M
,
R
F
7
9
,
8
4
e
p
i
s
o
d
e
s
4
7
(
1
4
)
y
,
2
9
/
5
0
3
5
(
4
4
%
)
4
6
(
5
8
)
d
N
o
t
d
e
s
c
r
i
b
e
d
2
4
%
n
o
i
m
p
r
o
v
e
m
e
n
t
,
3
0
%
p
a
r
t
i
a
l
r
e
s
o
l
u
t
i
o
n
1
1
%
i
n
f
a
r
c
t
s
i
n
s
a
m
e
a
r
e
a
s
i
n
v
o
l
v
e
d
i
n
P
R
E
S
e
p
i
s
o
d
e
R
e
c
u
r
r
e
n
t
P
R
E
S
(
n
=
4
)
,
r
e
c
u
r
r
e
n
t
s
e
i
z
u
r
e
s
(
n
=
5
)
P
r
e
e
c
l
a
m
p
s
i
a
/
e
c
l
a
m
p
s
i
a
6
N
o
t
d
e
s
c
r
i
b
e
d
N
o
t
d
e
s
c
r
i
b
e
d
N
o
t
d
e
s
c
r
i
b
e
d
R
o
t
h
2
0
1
0
P
r
e
c
l
a
m
p
s
i
a
/
e
c
l
a
m
p
s
i
a
,
H
E
,
C
T
,
A
D
,
o
t
h
e
r
2
5
,
2
7
e
p
i
s
o
d
e
s
3
5
(
2
3
)
y
,
7
/
1
8
2
0
(
8
0
%
)
6
.
2
(
0
.
2
2
5
.
7
)
y
1
.
5
T
,
T
1
/
T
2
,
F
L
A
I
R
,
D
W
I
2
8
%
C
o
m
p
l
e
t
e
r
e
c
o
v
e
r
y
o
r
c
l
e
a
r
i
m
p
r
o
v
e
m
e
n
t
o
f
W
M
L
s
M
i
l
d
v
i
s
u
a
l
a
b
n
o
r
m
a
l
i
t
i
e
s
a
f
t
e
r
7
6
d
w
i
t
h
p
a
r
t
i
a
l
r
e
m
i
s
s
i
o
n
M
R
I
w
i
t
h
a
n
e
w
I
C
H
(
n
=
1
)
,
r
e
c
u
r
r
e
n
t
P
R
E
S
(
n
=
2
)
,
h
y
p
e
r
t
e
n
s
i
v
e
d
i
s
e
a
s
e
(
n
=
1
2
)
P
r
e
e
c
l
a
m
p
s
i
a
1
N
o
t
d
e
s
c
r
i
b
e
d
N
o
t
d
e
s
c
r
i
b
e
d
N
o
t
d
e
s
c
r
i
b
e
d
E
c
l
a
m
p
s
i
a
9
T
A
B
L
E
2
.
(
C
o
n
t
i
n
u
e
d
)
P
R
E
S
-
A
s
s
o
c
i
a
t
e
d
C
o
n
d
i
t
i
o
n
P
R
E
S
C
a
s
e
s
,
N
M
e
a
n
/
M
e
d
i
a
n
A
g
e
(
S
D
/
I
Q
R
)
,
N
m
/
f
N
(
%
)
W
i
t
h
F
o
l
l
o
w
-
u
p
M
e
a
n
/
M
e
d
i
a
n
F
o
l
l
o
w
-
u
p
T
i
m
e
(
S
D
/
I
Q
R
)
M
R
I
S
e
q
u
e
n
c
e
s
%
o
f
N
W
i
t
h
I
m
a
g
i
n
g
A
b
n
o
r
m
a
l
i
t
i
e
s
a
t
F
o
l
l
o
w
-
u
p
S
p
e
c
i
f
i
c
F
o
l
l
o
w
-
u
p
I
m
a
g
i
n
g
A
p
p
e
a
r
a
n
c
e
C
l
i
n
i
c
a
l
S
y
m
p
t
o
m
s
a
t
F
o
l
l
o
w
-
u
p
L
i
m
a
n
2
0
1
2
(
R
e
f
.
2
2
)
P
r
e
e
c
l
a
m
p
s
i
a
/
e
c
l
a
m
p
s
i
a
,
I
M
,
S
O
T
,
B
M
T
,
i
n
f
e
c
t
i
o
n
,
A
D
,
C
T
,
o
t
h
e
r
9
6
3
6
(
2
3
6
2
)
y
,
3
1
/
6
5
5
3
(
5
5
%
)
2
6
(
9
5
2
)
d
1
.
5
/
3
T
,
T
1
/
T
2
,
F
L
A
I
R
,
D
W
I
4
3
%
H
i
g
h
e
r
b
l
o
o
d
p
r
e
s
s
u
r
e
a
s
s
o
c
i
a
t
e
d
w
i
t
h
i
n
c
o
m
p
l
e
t
e
r
e
s
o
l
u
t
i
o
n
(
P
=
0
.
0
0
1
)
;
f
o
c
a
l
g
l
i
o
s
i
s
,
i
n
f
a
r
c
t
i
o
n
,
p
o
s
t
h
e
m
o
r
r
h
a
g
i
c
r
e
s
i
d
u
a
,
a
t
r
o
p
h
y
,
l
a
m
i
n
a
r
n
e
c
r
o
s
i
s
N
o
t
d
e
s
c
r
i
b
e
d
,
r
e
c
u
r
r
e
n
t
P
R
E
S
(
n
=
1
)
P
r
e
e
c
l
a
m
p
s
i
a
/
e
c
l
a
m
p
s
i
a
S
e
e
L
i
m
a
n
2
0
1
2
(
R
e
f
.
2
8
)
S
e
e
L
i
m
a
n
2
0
1
2
(
R
e
f
.
2
8
)
S
e
e
L
i
m
a
n
2
0
1
2
(
R
e
f
.
2
8
)
S
e
e
L
i
m
a
n
2
0
1
2
(
R
e
f
.
2
8
)
L
e
g
r
i
e
l
2
0
1
2
P
r
e
e
c
l
a
m
p
s
i
a
/
e
c
l
a
m
p
s
i
a
,
H
E
,
C
T
,
A
D
,
I
M
,
o
t
h
e
r
7
0
3
6
(
2
5
5
2
)
,
2
5
/
4
5
4
9
(
7
0
%
)
9
0
d
N
o
t
d
e
s
c
r
i
b
e
d
5
5
%
N
o
t
d
e
s
c
r
i
b
e
d
S
o
m
e
l
e
v
e
l
o
f
f
u
n
c
t
i
o
n
a
l
i
m
p
a
i
r
m
e
n
t
(
n
=
3
7
)
,
d
e
a
t
h
(
n
=
1
1
)
P
r
e
e
c
l
a
m
p
s
i
a
/
e
c
l
a
m
p
s
i
a
1
6
N
o
t
d
e
s
c
r
i
b
e
d
N
o
t
d
e
s
c
r
i
b
e
d
S
o
m
e
l
e
v
e
l
o
f
f
u
n
c
t
i
o
n
a
l
i
m
p
a
i
r
m
e
n
t
(
n
=
2
)
S
t
u
d
i
e
s
i
n
c
l
u
d
i
n
g
o
t
h
e
r
n
o
n
o
b
s
t
e
t
r
i
c
c
o
n
d
i
t
i
o
n
s
P
r
a
s
a
d
2
0
0
2
C
h
i
l
d
r
e
n
w
i
t
h
h
y
p
e
r
t
e
n
s
i
o
n
1
8
,
1
6
w
i
t
h
P
R
E
S
1
1
(
4
)
y
,
1
3
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.
impaired cognitive functioning using objective neuro-
cognitive assessments.
45,46
Because persistent neuroimaging abnormalities have
also been described after nonobstetric conditions un-
derlying PRES, we reviewed the literature for cogni-
tive deficits in these conditions as well. Legriel
et al
42
found that the risk for an unfavorable functional
outcome (measured as the ability to return to occupa-
tional or academic activities with minor or no mental
deficits) was higher in nonobstetric causes of PRES
than after PRES in preeclampsia/eclampsia. Stroescu
et al
10
describe a 51-year-old woman with systemic lu-
pus erythematosusrelated PRES and hypertension.
She had hyperintense abnormalities on FLAIR MRI
bilaterally in the occipital lobes in the acute phase. At
neurocognitive examination 2 months later, she had
cognitive deficits; decreased working memory and vi-
sual attention; spatial perception deficits; and decreased
motor speed, visuospatial memory, and executive dys-
function. No follow-up MRI was available. Stott et al
19
identified 6 patients with PRES, 4 female and 2 male
patients, 2 of whom were 6-year-old children. One
child had no long-term sequelae after chemotherapy-
related PRES. The other, with PRES related to bone
marrow transplantation and cyclosporine treatment,
had persistent cognitive impairment, which the authors
did not otherwise specify. Although the effects of acute
hypertensive crises such as PRES in pediatric patients
are not exactly known, chronic hypertension without
PRES has been related to the development of subtle
cognitive dysfunction such as learning disabilities
and deficiencies in executive function, which may in-
terfere with normal developmental and/or learning
abilities.
47
It is unclear whether demonstrated cogni-
tive impairment in children with chemotherapy- or
hypertension-related PRES can be ascribed to the sin-
gle episode of PRES per se or rather to the effects of
the underlying disease and its treatment.
PRES AND THE DEVELOPMENT OF
EPILEPSY (SEIZURE DISORDER)
PRES in Preeclampsia/Eclampsia
It may be hypothesized that PRES in preeclampsia/
eclampsia in conjunction with persistent structural
damage may give rise to an epileptogenic focus and
delayed epilepsy. In the obstetric literature, mesial
temporal sclerosis has been described in several patients
after preeclampsia/eclampsia. Lawn et al
48
found that,
of 26 women undergoing anterior temporal lobectomy
for temporal lobe epilepsy (without other risk factors),
12 (46%) had a history of preeclampsia, and 9 of those
had had eclampsia. The period between the occurrence
of (pre)eclampsia and the onset of epilepsy was 1 month
to 2 years. None of these women had had seizures early
in life, febrile convulsions, intracranial infection, or
perinatal injuries, all of these typically associated
with subsequent temporal lobe epilepsy. Shah et al
49
followed 12 women who had eclampsia; 1 of them de-
veloped recurrent seizures within the first few months
but became seizure-free on phenytoin therapy. Kastrup
et al
50
describe 17 PRES patients who had an electro-
encephalogram (EEG) at the time of the acute episode,
3 of whom had preeclampsia and 3 had eclampsia.
None of those 6 women had seizures at 1 and 6 months
of follow-up. Of the 17 PRES patients, 10 had a repeat
EEG after 6 months, all without abnormalities.
PRES Associated With Autoimmune Disease
and/or Immunosuppressive Therapy
Baldini et al
51
describe a 21-year-old woman who
developed chronic epilepsy after PRES related to
tacrolimus use after liver transplantation for hepatitis
B liver cirrhosis. Six and 9 months after hospital dis-
charge, she had nocturnal generalized tonic-clonic
seizures. Although the frontal WML seen on MRI re-
solved within 1 year and the patient was seizure-free
by that time (while using oxcarbazepine), she demon-
strated persistent delta waves on the EEG. Solinas
et al
52
describe 3 children (a 10-year-old with acute
glomerulonephritis, an 8-year-old with Kawasaki dis-
ease, and a 3-year-old with nephrotic syndrome and
corticosteroid therapy) with refractory temporal lobe
epilepsy developing weeks to years after an episode
of PRES (hypertensive encephalopathy). They all
had hippocampal sclerosis, which is thought to be
an acquired lesion secondary to seizure-associated
damage or to vascular damage. In the study of Kastrup
et al,
50
the 2 patients with immunosuppressant-related
PRES did not have seizures or EEG abnormalities at
1 and 6 months of follow-up.
PRES Associated With Thrombotic
Thrombocytopenic Purpura
Belaramani et al
53
describe a 28-year-old man with
8 recurrent episodes of PRES; the first episode was
associated with thrombotic thrombocytopenic pur-
pura (TTP)hemolytic uremic syndrome. Subsequent
episodes were precipitated by severe hypertension
and not associated with metabolic abnormalities or
use of immunosuppressants. The patient developed
chronic epilepsy in the form of generalized tonic-
clonic seizures. Brain MRI (FLAIR) during one of the
PRES episodes showed edema in the parieto-occipital
areas, which resolved 3 months later, but scattered
subcortical T2 and FLAIR hyperintensities remained. It
should be noted that cerebral ischemic lesions are com-
mon in TTP without PRES.
37
PRES Associated With Malignant Disease
and Chemotherapy
A cohort of 56 children with chemotherapy-related
PRES was studied in which 55%had acute lymphoblas-
tic leukemia, 9% had acute myeloid leukemia, 13% had
non-Hodgkin lymphoma, and 23% had solid tumors.
40
Of these children, 8% were found to have developed
chronic epilepsy at long-termfollow-up. Lucchini et al
14
describe 12 children with chemotherapy-associated
PRES, 4 (33%) of whom developed unprovoked gener-
alized seizures (2 patients) and/or focal spikes on EEG
(2 patients) after 10 to 124 months. The underlying
disease was acute lymphoblastic leukemia in 9 patients
and Fanconi anemia, Langerhans cell hystiocytosis, and
immune hemolytic anemia in the others. In a study of
children being treated for acute leukemia, 19 (2.9%)
of 648 developed PRES.
41
Of these 19 patients, 5
showed persistent MRI abnormalities and 9 (50%) re-
quired long-term anticonvulsant therapy because of
continued epileptiform discharges on EEG or repeated
seizure episodes. Of these 9 patients, 6 underwent he-
matopoietic stem cell transplantation and 3 received
prophylactic intracranial irradiation therapy and/or
chemotherapy. Three of these 9 patients manifested
recurrent seizures although they were treated with
more than 3 different epileptic drugs. Belaramani
et al
53
describe 5 children with PRES, 4 of whom
had acute lymphoblastic leukemia and 1 had a central
nervous system germ cell tumor. All of them showed
good initial clinical recovery. Ultimately, 2 died of re-
current malignant disease and 1 developed refractory
epilepsy. This last patients MRI 7 years after the epi-
sode of PRES revealed right hippocampal sclerosis,
which, however, could be seizure related rather than
PRES related. In the study of Kastrup et al,
50
the 5
patients with chemotherapy-related PRES did not have
seizures or EEG abnormalities at 1 and 6 months of
follow-up. In the study of Khan et al,
54
the presence
of leukoencephalopathy in children with seizures asso-
ciated with hematological malignancies did not predict
the development of uncontrolled seizures in the subse-
quent years.
PRES AND VISUAL IMPAIRMENT
PRES in Preeclampsia/Eclampsia
Visual abnormalities in the acute phase of severe
preeclampsia and eclampsia are commonly described
as blurred vision, homonymous hemianopsia, visual
neglect, cortical blindness, or visual anosognosia.
These are thought to be due to the cerebral edema lo-
cated in the occipital (visual) cortex or the temporal
and parietal association cortices.
6
Although in most
patients, the impairment seems to be reversible, in
rare cases, permanent blindness has been described.
Moseman and Shelton
55
report a 21-year-old woman
presenting with blurred vision 1 day after cesarean
delivery for preeclampsia, which progressed to bilat-
eral blindness and persisted at 5-month follow-up. No
follow-up neuroimaging was performed. Cunningham
et al
56
performed a follow-up study of 10 women with
eclampsia and 5 women with preeclampsia without
seizures but with cerebral involvement in the form of
cortical blindness. The duration of blindness ranged
from 4 to 192 hours, but eventually, all showed self-
reported recovery of blindness and radiological recovery.
Bandyopadhyay et al
57
describe a 17-year-old pre-
eclamptic woman with reduced light perception, head-
ache, and confusion, 1 day postpartum. After treatment,
her vision returned to normal after 7 days. Wiegman
et al
9
investigated visual fields using automated perim-
etry and evaluated the presence of brain WMLs on MRI
in 47 women who had experienced eclampsia-related
PRES, on average, 10 years earlier. None of them dem-
onstrated visual field defects, whereas 36% of the
women had cerebral WMLs on MRI, predominantly
in the frontal lobes. Previously eclamptic women
reported a somewhat worse vision-related quality of
life compared with women who had normotensive
pregnancies. Those previously eclamptic women who
also had brain WMLs scored worse than those previ-
ously eclamptic without WMLs on MRI. Although
it may be hypothesized that WMLs may interfere with
higher-order visual functioning, no impairment on
neurocognitive tests of visual perception and only a
slight impairment in visuomotor speed are found after
preeclampsia/eclampsia.
46
PRES Associated With Autoimmune Disease
and/or Immunosuppressive Therapy
Lai et al
58
describe a 35-year-old woman with sys-
temic lupus erythematodes treated with cyclosporine
who developed a generalized tonic-clonic convulsion
and sudden binocular cortical blindness. Computed to-
mographic scan showed bilateral hypodense lesions in
the occipital lobe; on MRI, T2-hyperintense lesions in
the parieto-occipital regions were seen, not hypointense
on ADC images, consistent with vasogenic edema. She
had complete recovery of vision and of neuroimaging
findings at 4 months of follow-up.
PRES Associated With Malignant Disease
and Chemotherapy
Hemmaway et al
59
describe permanent cortical blind-
ness in a 60-year-old woman 1 year after PRES associ-
ated with chemotherapy for T-cell lymphoma. Magnetic
resonance imaging showed bilateral T2 hyperintense
lesions of the left occipital white matter in the acute
phase. No follow-up MRI was acquired.
PRES Associated With Acute Hypertension
(Hypertensive Encephalopathy)
Iwama et al
60
describe T2 hyperintense areas in the
posterior white matter at 5 months of follow-up in a
patient with hypertension-related PRES and bilateral
total cortical blindness. Kim et al
61
describe a 46-
year-old woman who developed intraoperative hy-
pertension with subsequent PRES after surgery for
intrauterine myoma. Visual acuity allowed light per-
ception only, but she quickly recovered to normal vi-
sion 1 day after treatment. Bandyopadhyay et al
57
describe a case of PRES related to acute hypertension
in a 75-year-old man with sudden, bilateral loss of
vision. He had extensive occipital lobe infarction on
CT imaging. After 6 months, visual acuity had
returned to 20/80 bilaterally without complete recov-
ery. Stott et al
19
describe 1 of 6 PRES patients with
residual left inferior quadrantanopia. This patient de-
veloped acute hypertension after acute hepatorenal
failure after a paracetamol overdose. Magnetic reso-
nance imaging revealed small areas of cerebral in-
farction in the right occipital lobe.
DISCUSSION
Posterior reversible encephalopathy syndrome is a
clinicoradiologic syndrome that has been associated
with numerous systemic conditions in both obstetric
(preeclampsia/eclampsia) and nonobstetric patients
of all age categories. We reviewed the literature to
identify possible long-term consequences of PRES,
particularly in obstetric compared with nonobstetric
patients. The literature mainly consists of small ob-
servational studies and case series, and follow-up
was often only short-term (several months). The re-
ported cases illustrate the heterogeneous pathology
that may underlie PRES, and this pathology itself
may induce (sub)clinical structural cerebral damage,
in addition to and independent of PRES. The published
data may represent an overestimation of the true inci-
dence of adverse sequelae after PRES because of pub-
lication bias. On the other hand, long-term sequelae
might be underreported because follow-up of PRES
patients is frequently lacking and there is no systematic
follow-up to elucidate potential subclinical effects.
Some general comments can be made.
On long-term follow-up, 41% and 37% of formerly
eclamptic and preeclamptic women, particularly those
with preterm preeclampsia, show WMLs on MRI com-
pared with 17% of age-matched women who had nor-
motensive pregnancies.
29,30
The pathogenesis of these
WMLs remains to be elucidated: they may be a direct
consequence of PRES or, alternatively, they may be
related to an increased propensity for cerebrovascular
disease in these women.
62,63
In nonobstetric PRES
patients, persistent MRI abnormalities, ranging from
WMLs and focal gliosis to intracranial hemorrhage
and infarction, are described more often, in 15% to
70%. However, these percentages need to be inter-
preted with caution. Hemorrhagic and major nonhe-
morrhagic stroke in nonobstetric PRES patients may
be considered separate consequences of the underlying
systemic pathology and, as such, occurring parallel to
PRES, rather than its consequence. From this perspec-
tive, the remarkably lowoccurrence of major clinically
recognizable sequelae after obstetric PRES and the
often less severe course of disease may illustrate the
fundamentally reversible nature of PRES. Severe pre-
eclampsia with headaches or visual disturbances and
eclampsia may very well be the forme fruste of PRES
because it very rarely occurs more than once, the un-
derlying condition (ie, pregnancy) is temporary, and
most women are otherwise healthy. This could explain
the more frequent occurrence of long-term sequelae in
nonobstetric PRES patients that may be more associ-
ated with the underlying cause than with the PRES
episode itself.
28,41
In formerly preeclamptic and eclamptic patients,
subjective cognitive problems have been reported,
7,8
whereas objective neurocognitive dysfunctioning on
neurocognitive tests cannot be demonstrated.
46
This
suggests that, at least, in women in their childbearing
age, PRES itself may not give rise to major structural
or functional damage, but its effect in later life is
unknown. Long-term cognitive dysfunctioning after
PRES seems to play a more prominent role in the
pediatric population. The developing pediatric brain
seems to be particularly vulnerable to hypertension
and seizure activity. The question is whether PRES
itself is the damaging factor in this pediatric popula-
tion or whether it is the underlying condition with its
associated effects.
Only 1 study describes a possible cause-and-effect
relationship between eclampsia and the subsequent
development of chronic epilepsy.
48
However, this
study used retrospective data, and it was not known
whether mesial temporal sclerosis was already pres-
ent before the eclamptic seizure. Most cases describ-
ing epilepsy after PRES were in children, especially
in those receiving chemotherapy. Here again, the un-
derlying condition, or even the medication giving rise
to PRES, might play a larger role in the development
of cognitive dysfunction and/or epilepsy than the
PRES episode in and of itself.
The visual abnormalities occurring during obstetric
and nonobstetric PRES seem reversible in most
cases, especially in cases when PRES was diagnosed
and managed in a timely manner. However, rare
cases have been described to progress to irreversible
(partial) blindness as a result of cerebral infarction.
Although preeclampsia/eclampsia-related PRES is
reversible in most cases, it is a serious and potentially
life-threatening obstetric emergency. Most women
will recover completely if provided adequate treat-
ment without delay. If not adequately treated, cere-
bral edema may lead to severe complications such
as intracerebral hemorrhage and major brain infarc-
tions and transtentorial herniation resulting in death.
Most reports suggest that late diagnosis or inadequate
therapy may influence the course of the disease be-
cause incomplete edema resolution may be associ-
ated with higher mean arterial pressure levels and
of longer duration.
42
Treatment of PRES, although not evidence based,
is aimed at removing the causative agent (in case of
pregnancy, delivery should be planned), blood pres-
sure management, and administration of anticonvul-
sive medication. In preeclampsia, in conjunction
with endothelial dysfunction, alterations in the cere-
bral circulation may occur despite minimal elevation
in blood pressure and a mild clinical picture. There-
fore, prompt diagnosis is needed in those women
who experience neurological symptoms, even with
blood pressure in the nonsevere range.
3
Neuroimaging
using MRI FLAIRand DWI sequences with ADCmap-
ping are best used for diagnosis and assessment of po-
tential irreversible damage due to cytotoxic edema.
Diffusion imaging may discriminate between poten-
tially irreversible lesions and those lesions that are re-
versible on follow-up MRI.
20
Because higher blood
pressure levels have been associated with incomplete
edema resolution,
21
adequate blood pressure control is
important. Lowering blood pressure in conjunction with
magnesium sulfate administration for prevention of (re-
current) eclamptic seizures and termination of preg-
nancy
28
are recommended.
64
We recommend follow-up MRI 6 months later in
women who experienced PRES in preeclampsia or
eclampsia to assess reversibility of edema, particularly
in those women who report long-term neurocognitive
problems or visual disturbances. Atypical radiological
findings such as hemorrhage and infarction may pre-
dict poorer outcome.
20
CONCLUSIONS
Long-term sequelae of both PRES in preeclampsia/
eclampsia and nonobstetric PRES-related conditions
have been poorly described so far. It seems that ob-
stetric PRES is associated with a less severe course
of disease and less frequent occurrence of long-
term adverse sequelae. In preeclamptic and eclamp-
tic patients, WMLs on MRI were found years later,
which may be related to common vascular risk
factors instead of the PRES episode per se. Formerly
preeclamptic and eclamptic women may report cog-
nitive difficulties, but these have not been confirmed
by objective neurocognitive testing so far. In con-
trast, several nonobstetric PRES-related conditions
have been described with long-term neuroimaging
abnormalities and overt cognitive problems, epilepsy,
or visual impairment. Whether these findings are re-
lated to the underlying cause of PRES rather than the
PRES episode itself remains to be established.
Attention needs to be paid to timely and adequate
treatment, as well as appropriate follow-up and sup-
port of PRES patients. With delayed treatment, PRES
may lead to cerebral infarction and hemorrhage.
Therefore, the need for early recognition and treat-
ment of PRES is important, although the clinical
findings of PRES are often nonspecific. Areas for fu-
ture research include identifying factors that predict
the development of PRES, individual components
of effective therapy, its recovery, and outcome.
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