Epilepsy & Behavior 48 (2015) 70–74

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Epilepsy & Behavior

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Seizure outcomes of posterior reversible encephalopathy syndrome and

correlations with electroencephalographic changes
Zhiyi Sha a,⁎, Brian P. Moran a, Alexander M. McKinney IV b, Thomas R. Henry a
a
Department of Neurology, University of Minnesota Medical School, Minneapolis, MN, USA
b
Department of Radiology, University of Minnesota Medical School, Minneapolis, MN, USA

a r t i c l e i n f o a b s t r a c t

Article history: Rationale: Seizures are among the most common clinical presentations of posterior reversible encephalopathy
Received 1 March 2015 syndrome (PRES). This syndrome has rarely been reported to cause chronic epilepsy or persistent cortical
Revised 16 April 2015 dysfunction. The prognostic value of EEG findings during PRES is unknown. We retrospectively evaluated EEG
Accepted 15 May 2015 characteristics in patients with PRES in a single medical center. We also evaluated the long-term outcome
Available online 10 June 2015
regarding seizure occurrence beyond the acute phase in these patients.
Methods: We searched a radiology database at the University of Minnesota from 1997 to 2012 to identify patients
Keywords:
Posterior reversible encephalopathy
with clinically and radiologically diagnosed PRES. Among the patients with PRES, we reviewed MRI images, EEG
syndrome (PRES) findings, clinical manifestations including seizure occurrences, and clinical outcomes beyond the acute phase.
Epilepsy Results: Seventy-five patients were included in the study. Fifty-eight out of seventy-five (77.3%) patients with
EEG PRES had seizures. A total of 48 EEG studies were performed in 38 patients. Generalized slowing was the most
MRI common EEG pattern. Among the 38 patients who had EEGs, 37 (97.3%) patients had diffuse or focal slowing
of the background, and 11 (28.9%) patients had IEDs. Four out of seventy-five (5.3%) patients had seizures later
than one month beyond their hospitalization for PRES. None of these 4 patients had seizures before the episode
of PRES. Two patients developed chronic epilepsy, with seizures occurring later than one year after the PRES.
Conclusion: Most patients who had seizures or who had epileptiform activities in EEG during PRES did not
subsequently develop chronic epilepsy. No patient developed chronic epilepsy in the absence of clinical seizures
during PRES. Posterior reversible encephalopathy syndrome may infrequently be associated with subsequent
development of symptomatic epilepsy.
© 2015 Elsevier Inc. All rights reserved.

1. Introduction and solid organ transplantation with immunosuppressant agents,

In 1996, Hinchey et al. first described reversible posterior leukoen-
cephalopathy syndrome, which is characterized by the clinical symptoms
of hypertension, headache, altered mental status, seizures and visual
disturbances associated with parietal and occipital white matter changes
on magnetic resonance imaging [1]. Different terms had been used to
describe this syndrome, including posterior reversible encephalopathy
syndrome (PRES), reversible posterior leukoencephalopathy, and
occipital parietal encephalopathy [2]. Posterior reversible encephalopathy
syndrome is the most commonly used name at the present time.
Posterior reversible encephalopathy syndrome is associated with a
variety of etiologies and predisposing factors, which include common
causes such as hypertension, preeclampsia–eclampsia, bone marrow
⁎ Corresponding author at: Department of Neurology, University of Minnesota, 717
Delaware St. S.E., Suite 510, Minneapolis, MN 55455, USA. Tel.: + 1 612 624 9025;
fax: +1 612 624 8111.
E-mail address: zysha@umn.edu (Z. Sha).
chemotherapy drugs, autoimmune diseases, and sepsis/infection. Less
common causes of PRES include hypercalcemia, Guillain–Barre
syndrome, intravenous immunoglobulin, tumor lysis syndrome, and
corticosteroid treatment [3–13]. Common neuroimaging findings in
PRES are usually subcortical edema in the posterior regions. However,
the term reversible posterior leukoencephalopathy is considered a
misnomer since this condition is not always reversible and is not
necessarily confined to the posterior regions of the brain. Both gray
matter and white matter can be affected [14]. This condition can be
seen in both adults and children [15,16]. The pathophysiology of PRES
is still poorly understood and controversial [5,17].
There are many detailed studies regarding the clinical aspect of PRES
[4,5,11,18–20]. However, the data regarding electroencephalographic
changes and seizure outcomes and their correlations with neuroimag-
ing studies are very limited. The aim of this study was to retrospectively
evaluate EEG characteristics in patients with PRES in a large single
medical center. We also evaluated the clinical outcome regarding
seizure occurrence beyond the acute phase in these patients and corre-
lations with EEG studies.

http://dx.doi.org/10.1016/j.yebeh.2015.05.027
1525-5050/© 2015 Elsevier Inc. All rights reserved.
 Z. Sha et al. / Epilepsy & Behavior 48 (2015) 70–74 71

2. Materials and methods Eclampsia/Postpartum

HTN
Immune suppressant + 3% Other
We retrospectively analyzed 91 patients diagnosed with PRES from
HTN 3%
1997 to 2012 at the University of Minnesota Medical Center from the
7%
radiology database. One of the authors (A.M.) prospectively maintained
a database for all patients with radiologically diagnosed PRES
from 1997 to 2012. These cases were retrospectively reviewed to deter-
mine clinical presentations, EEG findings, and radiological findings Unknown/Unclear
8%
(Supplementary Table 1). The inclusion criteria for the patients
with PRES were the following: (1) patients had to have a monophasic
illness with at least one of the common PRES presentations — (a) head- Cyclosporine
aches, (b) encephalopathy, (c) seizures, and/or (d) visual changes; (2) 34%
PRES on MRI diagnosed by a neuroradiologist from the University of Other immune
Minnesota Medical Center; and (3) clinical agreement by treating phy- suppressant
sicians, whose reports also were relied upon to determine the etiology. 17%
Seventy-five (50 females, 25 males, age: 3–80, average age:
39.2 years old) of the 91 (82.4%) patients screened met the inclusion Hypertensive
criteria. Thirty-eight of the 75 patients had at least one EEG study during emergency
the course of the PRES. Ten patients had a second EEG among these 38 28%
patients, and a total number of 48 EEGs were recorded (Supplementary
Table 2). Most had routine EEGs lasting about 30 min, but 7 patients had Fig. 1. Etiologies of patients with PRES.
prolonged EEG monitoring. An EEG was included in the data for acute
PRES if it was performed within 7 days prior to or 5 days after an MRI
confirming PRES. Furthermore, the patient's clinical course had to be than one month after hospital discharge. Two of these 6 patients had re-
consistent with the ongoing presence of PRES at the time of the EEG. current seizures only at the time of recurrent PRES due to immunosup-
After MRI confirmation of PRES, treatment steps would take place to pressive agents that were continued based on medical necessity
address it, so a shorter period of 5 days following the MRI was used to (avoidance of transplanted organ rejection). One of these 2 patients
include EEG studies as being the acute phase. also had had a seizure prior to PRES that was attributed to hypoxemia.
Each patient's clinical presentation and causal factors were identified. Four (5.3%) patients had seizures one month after discharge without
Electroencephalography studies were recorded with standard bipolar recurrent PRES or other new insults. These were patients 8, 32, 34, and
montage, with electrodes placed according to the international 10–20 72. Patients 8 and 34 developed chronic epilepsy and required antiepi-
system. Electroencephalography patterns were interpreted by faculty leptic drug treatment chronically after PRES.
epileptologists at the University of Minnesota Medical Center, who
were fellowship-trained in EEG and epilepsy. Electroencephalography
3.2. EEG findings
was analyzed for background activities, focal or generalized slowing
and spikes, and other abnormalities. These EEGs were reviewed, and, in
Among the 58 patients with seizures, a total of 48 EEG studies were
each case, previous EEG interpretations were confirmed by the current
performed in 38 patients during the hospital stay. Only one of these 48
investigators. Spikes, spike–wave discharges, and sharp waves were
EEGs was found to be normal (Table 1). Generalized slowing of the
terms used to describe epileptiform activities in some references.
background activities was the most common pattern (Fig. 2). Four
Interictal epileptiform activities (IEDs) are used in this study for epilepti-
(8.3%) patients had focal but symmetric slowing. Two patients had
form activities.
focal slowing and periodic lateralized epileptiform discharges (PLEDs).
Seizure occurrence and semiology were based on clinical description
Two patients had diffuse slowing with triphasics. One patient had
in the chart and came from a variety of sources including associates/
focal but symmetric slowing with IEDs. One patient had focal slowing
family of the patients, nursing staff, and physicians. Epilepsy was
and IEDs (Fig. 3). One patient had only focal slowing. Taken together,
defined as two or more unprovoked seizures that occurred at greater
among the 38 patients who had EEGs, 37 (97.3%) patients had diffuse
than one month after discharge.
or focal slowing of the background, while 11 (28.9%) patients had IEDs.
3. Results
3.3. Radiological abnormalities
Among these 75 patients with PRES, the clinical presentations
required for inclusion were seizures, headaches, encephalopathy, and As it was required by the inclusion criteria, all patients in the study
visual disturbances. The etiologies of the PRES were identified by had an MRI of the brain during PRES. During the course of PRES, 26/75
treating physicians as the following: cyclosporine (34.7%), hypertension (34.7%) patients had focal lesions beyond the vasogenic edema that
(28.0%), other immunosuppressive agents (17.3%), hypertension plus
immunosuppressive agents (6.6%), eclampsia and postpartum
Table 1
hypertension (2.7%), lupus (1.3%), and renal failure (1.3%). The etiology EEG studies of patients with PRES.
was unknown in 8.0% of the cases (Fig. 1).
EEG findings No. of EEGs

3.1. Seizures during and after PRES Diffuse slowing alone 25

Diffuse slowing and sharps/spikes 11
Diffuse slowing with triphasics 2
During the course of PRES, 58 (77.3%) out of 75 patients suffered at
Focal but symmetric slowing 4
least one seizure. Most of the seizures were generalized tonic–clonic Focal but symmetric slowing with sharps/spikes 1
seizures. In addition to single or recurrent generalized tonic–clonic PLEDs and focal slowing 2
seizures, 3 patients had focal motor seizures with secondary generaliza- Focal spikes and focal slowing 1
tion, 2 had complex partial seizures, 2 had convulsive status epilepticus, Focal slowing 1
Normal 1
and 1 had focal motor seizures. Six patients of the 75 had seizures later
72 Z. Sha et al. / Epilepsy & Behavior 48 (2015) 70–74
Fig. 2. MRI and EEG changes of patients with PRES. Despite imaging findings (T2 hyperintensities on FLAIR) typically localized to the posterior regions of the brain in PRES, the characteristic
EEG feature in our study was diffuse slowing consistent with the clinical presentation of encephalopathy. Seen here are the studies of patient 73 who developed PRES following a bone
marrow transplant for acute myelogenous leukemia (AML) while on treatment with tacrolimus.
typifies the condition. These focal lesions included 15/75 (20%) patients
with infarcts and 11/75 (14.7%) patients with hemorrhages.
Only 22 (29%) patients had follow-up MRI studies. With the
resolution of the PRES, 3 patients were found to have focal atrophy in
previously affected areas, and one had cortical laminar necrosis.
3.4. Correlations of epilepsy with EEG and imaging findings
Of the 4 patients who had seizures occurring more than one month
after discharge, patient 8 had 2 foci of restricted diffusion on MRI during
PRES and diffuse slowing with a sharp wave on EEG; patient 32 had no
focal lesions on MRI besides edema, but no EEG was performed during
PRES; patient 34 had no focal lesions on MRI besides edema and diffuse
slowing or diffuse slowing with triphasics on two EEGs during PRES;
and patient 72 had punctate infarcts and a larger right ACA territory in-
farction on MRI with diffuse slowing on EEG during PRES. Two patients,
patient 8 and patient 34, developed chronic epilepsy after the PRES. Pa-
tient 8 had diffuse slowing, and one sharp wave in her EEG and the MRI
of the brain had foci of restricted diffusion during the acute phase of
PRES. Three follow-up post-PRES EEGs while the patient was on AEDs
were either normal or just showed diffuse slowing of the background
activities. A follow-up MRI of the brain was normal three years after
PRES. Patient 34 had (1) diffuse slowing with triphasics and (2) diffuse
slowing alone in her first two EEGs during the acute phase of PRES. A
follow-up EEG after the acute phase showed epileptiform activities bi-
laterally in the posterior quadrants affected by the PRES. The MRI
showed only edema during the PRES, but a follow-up MRI showed
areas of encephalomalacia over the parietal/occipital regions that had
been affected by PRES. No particular EEG finding was useful in the pre-
diction of subsequent seizures.
4. Discussion
The clinical manifestations of PRES include headaches, encephalopa-
thy, seizures, vomiting, and visual disturbances. Imaging studies of these
patients show bilateral occipital vasogenic edema which resolved after
the acute phase of this syndrome. The underlying pathophysiology is
generally thought to be the result of endothelial cell dysfunction and
loss of cerebral vascular autoregulation in the setting of elevated system-
ic blood pressure or the presence of neurotoxic agents. In recent years,
the term posterior reversible encephalopathy syndrome (PRES) has
been considered a misnomer as this condition is not always reversible,
is not always confined to the posterior regions of the brain, and can affect
both the white matter and the gray matter [14].
Over the years, the clinical and radiographic changes of PRES have
been well described [17,21–26]. However, studies of the electroenceph-
alographic findings and seizure prognosis have not been extensively
reported. Most of these publications were single-case reports, in spite
of the fact that seizure is a common manifestation in PRES [19,27–29].
Natsume et al. reported EEG findings in three children who suffered
posterior reversible encephalopathy associated with immunosuppres-
sants [28]. The EEG showed continuous focal discharges in the
acute period. Electroencephalography findings normalized after the
clinical manifestation had disappeared without additional anticonvul-
sant treatment. Although the MRI findings in these patients were
more diffuse bilaterally including the frontal lobes, the seizures and
EEG abnormalities were more focal in the occipital area. Other reports
have shown that periodic lateralized epileptiform discharges (PLEDs)
may be the initial electrographic pattern of PRES [30] or that PLEDs
may be the EEG manifestation of recurrent episodes of PRES [29].
A more recent report from Kastrup et al. [31] studied EEG findings in
17 patients with PRES who suffered from seizures. EEG showed diffuse
slowing in 13 (76.5%) of 17 patients, and epileptiform activities with
focal discharges and PLEDs were found in 2 (11.8%) patients.
In our study, 97.9% of the EEGs were abnormal during the course of
PRES. The most common EEG pattern in these patients with PRES was
generalized slowing of the background activities (52.1%). A total of
79.1% of the EEGs had diffuse slowing of the background or diffuse
slowing with sharp waves, and 27.1% of the EEGs had sharps and/or
spikes. Most of the patients who had sharps and/or spikes during
acute PRES (12/13) did not develop epilepsy after the acute phase of
PRES. These findings demonstrated that EEG had limited value in
long-term prognostication and should not be used to predict the devel-
opment of future chronic epilepsy.
 Z. Sha et al. / Epilepsy & Behavior 48 (2015) 70–74
Fig. 3. Right temporal/parietal spike–wave discharges in patient 75 during acute PRES, who did not develop epilepsy. The presence of epileptiform activity during acute PRES was not
predictive of epilepsy outcome.
In Kastrup's study [31], all seizures occurred in the early stage of PRES
after the disease onset and terminated spontaneously or under
antiepileptic therapy during the first 24 h. No patient suffered seizures be-
yond the first 24 h, and chronic epilepsy was not seen in their group. The
authors concluded that chronic epilepsy does not result from PRES and
that long-term antiepileptic treatment is not warranted. A recent long-
term PRES follow-up study followed a group of 25 patients for a mean
period of over 6 years. In this group, acute symptoms resolved after an av-
erage of 7.5 days. Most had resolution of abnormalities on MRI after
41 days. Recurrence of PRES was found in 2 patients. Although 84% of
the patients developed generalized seizures as their initial presentation,
no patients developed chronic epilepsy in their long-term follow-up [32].
In contrast, in our study, of the 58 patients who presented with
seizures at the time of PRES, 4 (6.9%) patients had seizures beyond
one month after hospital discharge, including two patients with sei-
zures occurring longer than one year following PRES. Patient 8 had
one sharp wave in her EEG during the acute phase; 3 follow-up EEGs
were either normal or only had diffuse slowing. Despite this, this patient
had seizure recurrence one month after being taken off AEDs, 3 years
after the initial diagnosis of PRES. Patient 34 had diffuse slowing and
triphasic waves during the acute phase of PRES; a follow-up EEG
showed epileptiform activities from the areas affected by PRES. These
findings suggest that although EEG has limited predictive power regard-
ing future seizures, anyone with epileptiform activities on EEG follow-
ing PRES should be carefully monitored for seizure recurrence and
73
should probably be maintained on AEDs. These data also suggest that
PRES can be the cause of chronic epilepsy, although this is uncommon.
Interestingly, one recent case report showed that an eight-year-old
female developed pharmacoresistant epilepsy after PRES. Cerebral MRI
three years later after the diagnosis of PRES showed hippocampal
sclerosis which was not present on the initial MRI when she was first
diagnosed with PRES [33].
A more recent study by Datar et al. looked at the long-term risk of
seizures and epilepsy in patients with PRES. Out of the 127 patients
who were diagnosed with PRES, 3 (2.3%) patients had unprovoked
seizures during the follow-up period, and only one (0.7%) patient was
considered to have developed epilepsy [34]. These results are consistent
with the findings in this study.
Hypertension, eclampsia, renal failure, and immunosuppressive
treatment are the common causes for PRES [1,35]. Among these causes,
hypertension was thought to be the most common etiology. In some
series, the moderate-to-severe hypertension was reported in as many
as 75% of the cases of PRES [4,5]. Our results are consistent with previous
studies which showed that PRES occurs in a wide range of disorders and
predisposing conditions. However, in our study, the most common eti-
ology was an immunosuppressant alone (52.0%); hypertension alone
accounted for only 28.0% and eclampsia/postpartum hypertension for
2.7%. This is probably due to the fact that we have a major transplant
center in our hospital and that there is a large number of patients who
were or are currently on immunosuppressive agents.
74 Z. Sha et al. / Epilepsy & Behavior 48 (2015) 70–74
Magnetic resonance imaging study allows better characterization
and recognition of PRES than computed tomography [22]. The typical
MRI changes in PRES include increased signal changes in T2 and fluid at-
tenuated inversion recovery (FLAIR) images with increased apparent
diffusion coefficient (ADC) values in the posterior regions of the cerebral
hemispheres, which indicate the presence of vasogenic edema [4,22,23,
26]. In recent years, atypical radiographic changes in PRES were increas-
ingly recognized [17,20,36,37]. Although the posterior regions are com-
monly affected in PRES, involvement of other regions such as frontal
lobe or cerebellum is frequent. Microhemorrhages may be present in
over half of the patients with PRES based on susceptibility weighted
images (SWIs), and the potential for such lesions to lead to epilepsy is
not yet described [38].
To date, the correlations between imaging findings and seizure
outcome have been poorly described [20,22,36]. In the four patients
who had seizures one month after the acute phase, two had infarction
during the acute phase, and one had focal atrophy on follow-up
imaging. One patient had only vasogenic edema initially, and no residu-
al lesion on follow-up MRI. Most patients with acute/subacute focal
lesions such as infarction, hemorrhage, laminar necrosis, or focal
atrophy did not develop chronic epilepsy beyond the acute phase of
PRES. Our study has indicated that there was no significant correlation
between any particular MRI findings and any particular EEG findings
or the likelihood of seizure recurrence.
To our knowledge, this is the first large single center study of PRES
that shows that PRES can be a cause of chronic epilepsy, with EEG and
radiological correlations. The main limitation of this retrospective
study is that an EEG study was obtained only in half of the patients
with PRES. There might be a selection bias for patients who underwent
EEG recording, such that patients with seizures or more severe PRES
might be more likely to be referred for EEG. The patients with seizures
were identified only because of focal or generalized convulsive seizures.
Patients with more subtle clinical seizures might have been missed.
Some of the patients were maintained on AEDs, which could have
masked underlying epileptogenesis.
Supplementary data to this article can be found online at http://dx.
doi.org/10.1016/j.yebeh.2015.05.027.
Disclosure
We have no conflicts of interest to disclose.
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