Regional Distribution of Cerebral White
Matter Lesions Years After Preeclampsia
Marjon J. Wiegman, MD, PhD, Gerda G. Zeeman, MD, PhD, Annet M. Aukes, MD, PhD,
Antoinette C. Bolte, MD, PhD, Marijke M. Faas, PhD, Jan G. Aarnoudse, MD, PhD,
and Jan C. de Groot, MD, PhD
OBJECTIVE: To assess the distribution of cerebral white
matter lesions in women who had eclampsia, preeclamp-
sia, or normotensive pregnancies. The pathophysiology of
these lesions, more often seen in formerly eclamptic and
preeclamptic women, is unclear but may be related to
a predisposition for vascular disease, the occurrence of the
posterior reversible encephalopathy syndrome, or both
while pregnant. Assessing the distribution of such lesions
may give insight into their pathophysiology and possible
METHODS: This retrospective cohort study determined
the presence, severity, and location of white matter
lesions on cerebral magnetic resonance imaging scans
of 64 formerly eclamptic, 74 formerly preeclamptic, and
75 parous control women.
RESULTS: Formerly preeclamptic and eclamptic women
have white matter lesions more often (34.4% [n547]
compared with 21.3% [n516]; P,.05) and more severely
(0.07 compared with 0.02 mL; P,.05) than parous women
in a control group. In all women, the majority of lesions
was located in the frontal lobes followed by the parietal,
insular, and temporal lobes.
CONCLUSION: White matter lesions are more common
in women with prior pregnancies complicated by pre-
eeclampsia or eclampsia compared with parous women
in a control group. In no group does regional white
matter lesion distribution correspond to the occipitopar-
ietal edema distribution seen in posterior reversible
(Obstet Gynecol 2014;123:790–5)
LEVEL OF EVIDENCE: II
eclamptic and preeclamptic women compared with
women after normotensive pregnancies.1,2Although
the pathogenesis of white matter lesions remains to
be elucidated, the increased propensity for cerebrovas-
cular and cardiovascular disease in formerly pre-
eclamptic women3may be an associated factor. We
hypothesize that an episode of posterior reversible
encephalopathy syndrome, which is considered the
underlying cause of the neurologic symptoms in
eclamptic as well as some preeclamptic patients, may
play an additional role.4In posterior reversible enceph-
alopathy syndrome, severe vasogenic edema has been
suggested to potentially progress to such an extent that
regional cerebral perfusion decreases, leading to areas
of cytotoxic edema, infarction, and development of
white matter lesions in the long term.5,6
In elderly individuals, white matter lesions are
associated with cognitive decline and dementia7and
are mainly located in the frontal and parietal lobe.8–10
Although impaired subjective cognitive functioning in
formerly eclamptic women has been reported,11,12no
significant differences were found for objective meas-
ures of sustained attention and executive functioning
n previous studies an increased prevalence of cere-
bral white matter lesions was found in formerly
From the School of Behavioural and Cognitive Neurosciences, Department of Obstetrics
and Gynecology, the Division of Medical Biology, Department of Pathology and Medical
Biology, and the Department of Radiology, University of Groningen, University Medical
Center Groningen, and the Department of Obstetrics and Gynaecology, VU University
Medical Center Amsterdam, Amsterdam, The Netherlands.
The authors thank Jim van Eyck for contributing to the recruitment of partic-
ipants and Henk Groen for his help with the statistical analyses.
Corresponding author: Marjon J. Wiegman, MD, PhD, University Medical
Center Groningen, Department of Dermatology, Hanzeplein 1, 9700 RB
Groningen, The Netherlands; e-mail: email@example.com.
The authors did not report any potential conflicts of interest.
© 2014 by The American College of Obstetricians and Gynecologists. Published
by Lippincott Williams & Wilkins.
VOL. 123, NO. 4, APRIL 2014OBSTETRICS & GYNECOLOGY
after eclampsia.13Moreover, in former patients with
posterior reversible encephalopathy syndrome, per-
manent clinical symptoms have been found including
impaired self-perceived as well as objective neurocog-
nitive functioning and visual disturbances,11,12,14–16
partly thought to be related to permanent cerebral
lesions. However, the clinical implications of white
matter lesions in formerly preeclamptic and eclamptic
women remain so far unclear.
To get insight into the pathophysiology and possi-
ble consequences of white matter lesions, this study
assessed the distribution of such lesions in women who
had eclampsia or preeclampsia compared with women
who had normotensive pregnancies several years prior.
MATERIALS AND METHODS
Participants were enrolled in this retrospective cohort
study as part of ongoing follow-up studies assessing
cerebral long-term consequences of preeclampsia and
eclampsia such as white matter lesions and neuro-
cognitive functioning.1Three groups of women were
recruited for these studies, ie, formerly eclamptic, for-
merly preeclamptic, and parous control women.
Women with a diagnosis of eclampsia in their
medical history between 1988 and 2005 were identified
from the electronic admission, diagnosis, and delivery
databases of the University Medical Center Groningen.
Recruitment and selection criteria have been published
previously.1,2In the meantime, additional formerly
eclamptic women have been recruited to participate in
our follow-up studies through collaboration with two
other tertiary referral centers: the VU University Medical
Center Amsterdam and Isala Clinics Zwolle. In addition,
six formerly eclamptic women who delivered in other
hospitals and who had heard about this study requested
to participate in the current study, which was allowed.
Recruitment and selection criteria of participating
women with a diagnosis of preeclampsia or normoten-
sive pregnancies in their medical history were reported
previously.2Briefly, medical records of formerly eclamp-
tic and preeclamptic women were reviewed for accurate-
ness of diagnosis and to extract clinical and demographic
characteristics. Both eclampsia and preeclampsia were
defined according to the definition of the International
Society for the Study of Hypertension in Pregnancy.17
Parous women in the control group were recruited
through either the department’s electronic delivery data-
base or among hospital employees and their family
members. Their records were evaluated to confirm that
the pregnancy was indeed uneventful and normotensive.
Exclusion criteria included contraindication for magnetic
resonance image (MRI) scanning, a history of epilepsy,
cerebrovascular accident, demyelinating disorders, intra-
cranial infections or any cranial neurosurgical procedure,
or the inability to understand Dutch. Only women who
did not meet any of the exclusion criteria were invited to
participate in the current study by mail.
After the MRI procedure and after a period of
rest, blood pressure was measured manually using
a aneroid sphygmomanometer. Patients with a systolic
blood pressure of 140 mmHg or greater, diastolic
blood pressure 90 mmHg or greater, or both or
currently using antihypertensive medication or both
were designated as currently hypertensive.18
Approval for this project was obtained from the
Medical Ethics Committee of the University Medical
Center Groningen and all participants signed informed
Detailed MRI study protocols have been pre-
viously described.1Briefly, participants underwent
MRI on a 3-T MRI system using the following se-
quences: T1, proton density, T2, and fluid-attenuated
inversion recovery using parameters as described pre-
viously.1Transverse slice thickness was 5 mm with
a 20% interslice gap. The presence, size, and number
of white matter lesions were rated by an experienced
neuroradiologist, who was blinded for patient category
as previously described.1,19White matter lesions were
considered present if hyperintense on fluid-attenuated
inversion recovery, T2- and proton density-weighted
images and not hypointense on T1-weighted images.
Subcortical white matter lesions were categorized
according to their largest diameter as small (less than
3 mm), medium (3–10 mm), or large (greater than
10 mm). The number of lesions was evaluated per size
category for the following locations: frontal, parietal,
temporal, occipital, insular, brainstem, and cerebellum.
Considering them spherical with a fixed diameter per
size category, a total approximated volume for subcor-
tical white matter lesions was determined.
For evaluation of prevalence and mean volume of
lesions in each group, correction for inclusion of partial
volume was performed as previously described.2Briefly,
for each participant, an arbitrary two small lesions were
subtracted from the total number of small lesions. This
means that women with only two small lesions or less
were considered as white matter lesion–negative. Correc-
tion for partial volume was not possible for evaluation of
regional distribution because it is not feasible to deter-
mine from which brain region(s) the partial volume cor-
rection (ie, two small lesions) should be subtracted if
a woman demonstrates small lesions in more than one
region. Therefore, prevalence of white matter lesions
according to brain region was evaluated in lesion-
positive women only with inclusion of all lesions,
ie, without correction of partial volume.
VOL. 123, NO. 4, APRIL 2014Wiegman et alCerebral Lesions After Preeclampsia and Eclampsia
Descriptive statistics such as demographic infor-
mation are presented as means6standard deviations
for continuous variables and percentages for dichoto-
Demographic data were compared among for-
merly eclamptic, preeclamptic, and control women
using analysis of variance for normally distributed data,
or Kruskal-Wallis test for data that were not normally
distributed. Dichotomous variables, ie, presence of
white matter lesions, current hypertension, current
smoking, and nulliparity, were compared between the
groups using x2with pair wise x2as the post hoc test.
Lesion volume between formerly (pre)eclamptic and
control women was compared using the Mann-
Whitney test. To evaluate differences in presence of
white matter lesions between brain regions, the propor-
tion of women with lesions in the frontal lobe was
compared with the proportion of women with lesions
in the other brain regions using McNemar’s test.
Differences were considered statistically signifi-
cant at P#.05. For evaluating differences in presence
of white matter lesions between brain regions, a Bon-
ferroni correction was applied to this a level. Data
analyses were performed using SPSS statistical pack-
age for Windows 8.
The recruitment and inclusion process of the formerly
preeclamptic women (n574) and the women who had
normotensive pregnancies (n575) has recently been
described in a report on presence and lesion load of
white matter lesions.2The group of formerly eclamptic
women has been expanded since our last report,1in
which neuroimaging data of 39 formerly eclamptic
women were presented. Therefore, we now provide
detailed description of the recruitment of the entire
group of women who had eclampsia. In total, 137 for-
merly eclamptic women were identified. Six of these
women were excluded, one because diagnosis of
eclampsia could not be confirmed, another because of
a history of a cerebrovascular accident, and a third as
a result of inability to understand Dutch. In addition,
three women had died in the interim, two of whom
were the result of cerebral complications resulting from
eclampsia and one as a result of gynecologic cancer. Of
the remaining 131 formerly eclamptic patients, 69 could
be reached and were willing to participate. Six of them
were subsequently excluded as a result of contraindica-
tions for MRI scanning. Three of the 63 women who
were included in the formerly eclamptic group had not
experienced tonic–clonic seizures. These three, how-
ever, had experienced generalized myoclonic twitches
while conscious, suggesting cerebral involvement.
Therefore, for this study, we describe the MRI findings
of a total of 63 formerly eclamptic, 74 formerly pre-
eclamptic, and 75 parous control participants.
Table 1 shows baseline characteristics of the study
participants. Mean age at the time of participation was
similar for all groups; all groups were in their late 30s.
However, elapsed time since the index pregnancy was
longer for the formerly eclamptic women (7.664.7
years) compared with both formerly preeclamptic
women (5.264.1 years) and parous women in the con-
trol group (5.063.3 years). Furthermore, the percent-
age of women who were nulliparous at the time of the
index pregnancy differed between the groups with
most nulliparous women in the formerly eclamptic
group (82.5%) followed by formerly preeclamptic
(67.6%) and control women (46.7%). Estimated gesta-
tional age at delivery was more than 6 weeks shorter in
formerly eclamptic and preeclamptic women com-
pared with parous women in the control group. In
addition, as expected, birth weight of the neonate was
approximately 45% lower in the formerly eclamptic
and preeclamptic group than the control group.
Current weight and the percentage of women
who currently smoke were comparable among the
three groups. Systolic and diastolic blood pressures
were higher and hypertension occurred four times
more often in formerly eclamptic and preeclamptic
women than in parous women in the control group.
Although formerly eclamptic (n520 [31.7%]) and
preeclamptic women (n527 [36.5%]) appeared to
have subcortical white matter lesions more often than
parous women in the control group (n516 [21.3%]),
these differences did not reach significance (P5.11).
However, when grouped together, the (pre)eclamptic
group had lesions significantly more often than parous
women in the control group (34.4% compared with
21.3%; P,.05). In addition, lesion load was more than
threefold in formerly preeclamptic and eclamptic
women (mean volume 0.07 mL, range 0.00–2.35 mL)
compared with women in the control group (mean
volume 0.02 mL, range 0.00–0.13 mL, P,.05).
The cerebral regional distribution of lesions in
white matter lesion–positive women was comparable
for all groups (Fig. 1). In all three groups, the majority
of lesions was located in the frontal lobes (P,.005;
frontal lobe compared with any other brain region).
In the formerly preeclamptic group, all women with
lesions (n527) demonstrated these in the frontal
lobes. Eighty-five percent (n517) of the formerly
eclamptic women with lesions had these lesions in
the frontal lobe; for control participants, this was
87.5% (n514). The parietal lobe was the second most
affected region by white matter lesions, that is, in 35%
Wiegman et alCerebral Lesions After Preeclampsia and Eclampsia OBSTETRICS & GYNECOLOGY
of formerly eclamptic (n57), 29.6% of formerly pre-
eclamptic (n58), and 25% of control women (n54).
In addition, three formerly preeclamptic women
(11.1%) and one control woman (6.3%) demonstrated
lesions in the temporal lobes. The insular lobes were
affected by white matter lesions in four formerly
eclamptic women (20.0%) and two women in the con-
trol group (12.5%). One formerly eclamptic woman
(5.0%) had a lesion located within the cerebellum.
White matter lesions in more than one brain region
were observed in 40.0% of the formerly eclamptic
(n55), 33.3% of formerly preeclamptic (n59), and only
in 25.0% of control women (n54). In all participants,
except for three formerly eclamptic and two women in
the control group, lesions in the parietal, temporal, or
insular lobe and cerebellum were accompanied by le-
sions in the frontal lobes. None of the participants
showed involvement of the occipital lobe or brainstem.
Periventricular white matter lesions were present
in only one formerly eclamptic woman. She did not
demonstrate any subcortical white matter lesions. In
five formerly preeclamptic women, periventricular
lesions were observed. These women all demonstrated
subcortical lesions in addition. None of the control
women had periventricular white matter lesions. In all
women demonstrating periventricular white matter
lesions, these lesions were considered mild, a pencil
thin lining surrounding only part of the ventricles.
In the formerly eclamptic group, one woman
demonstrated a lacunar infarct and two women had
cortical infarcts. Two of these women also demon-
strated subcortical white matter lesions. In the for-
merly preeclamptic group, two women had lacunar
infarcts and one woman demonstrated a cortical
infarct. These three women all had subcortical white
matter lesions in addition to the infarcts. None of the
control women had cerebral infarcts.
The pathophysiology of white matter lesions in
formerly preeclamptic and eclamptic women remains
speculative and by assessing their distribution, we
Frontal ParietalTemporalInsular Cerebellum
Presence of white matter lesions (%)
Fig. 1. Regional distribution of cerebral white matter lesions
in white matter lesion–positive women. Presence of white
matter lesions (with 95% confidence interval) per brain
region for white matter lesion–positive women in the parous
control group, formerly preeclamptic group, and formerly
eclamptic group. Women who did not demonstrate white
matter lesions are not included in this figure. No white
matter lesions were observed in the occipital lobe and
brainstem in any of the groups. *P,.005 compared with any
other brain region of the same group.
Wiegman. Cerebral Lesions After Preeclampsia and Eclampsia.
Obstet Gynecol 2014.
Table 1. Participant Characteristics
Women in the Control
Group (n575) Preeclampsia (n574)Eclampsia (n563)
Current age (y)
Elapsed time (y)
Estimated gestational age at delivery (wk)
Neonatal birth weight (g)
Current systolic BP (mmHg)
Current diastolic BP (mmHg)
Current hypertension (n)
Current weight (kg)
Current smoking (n)
White matter lesions present (n)
BP, blood pressure.
Data are mean6standard deviation or % (n of women).
* P,.01 compared with those in the control group and preeclampsia.
†P,.001 compared with preeclampsia and eclampsia.
‡P,.01 compared with preeclampsia and P,.001 compared with eclampsia.
§P,.05 compared with eclampsia.
kP,.01 compared with preeclampsia and P,.05 compared with eclampsia.
VOL. 123, NO. 4, APRIL 2014Wiegman et alCerebral Lesions After Preeclampsia and Eclampsia
aimed to provide insight into their development.
Previously, we have hypothesized that such white matter
lesions may be related to posterior reversible encepha-
lopathy syndrome.1,2In posterior reversible encephalop-
athy syndrome, an acute increase in blood pressure may
cause loss of cerebral autoregulation, resulting in blood–
brain barrier disruption, vasogenic edema formation, and
neurologic symptoms.20–22Severe vasogenic edema in
the acute phase of posterior reversible encephalopathy
syndrome may reduce blood flow to ischemic levels,
resulting in cytotoxic edema.5This may later appear
as infarction or white matter lesions on MRI.5,6We
expected a similar white matter lesion distribution to that
of cerebral edema in posterior reversible encephalopathy
syndrome. However, although the edema in posterior
reversible encephalopathy syndrome is typically located
in the occipitoparietal lobes,23this study demonstrates
only few women with lesions in the posterior brain re-
gions. In fact, the majority of lesions were located in the
frontal lobes. Moreover, this distribution was similar
between women who had posterior reversible enceph-
alopathy syndrome, ie, the formerly eclamptic women,
and women without posterior reversible encephalopa-
thy syndrome, ie, the parous women in the control
group. Therefore, a direct causal relationship between
the cerebral edema of posterior reversible encephalop-
athy syndrome and white matter lesions in formerly
preeclamptic and eclamptic women seems unlikely.
Alternatively, in the general population, the pres-
ence of hypertension is associated with cerebral white
matter lesions,24–26which may also explain the higher
prevalence of such lesions in our preeclamptic and
eclamptic women. Preeclampsia is associated with an
increased risk for vascular disease later in life, including
hypertension, ischemic and hemorrhagic stroke, and
ischemic heart disease.3In this context, the cardiovascu-
lar and metabolic demands of normal pregnancy are
considered a physiologic “stress test.”27Predisposed
women fail this test and develop preeclampsia during
pregnancy, thereby revealing their increased lifetime risk
for cerebrovascular and cardiovascular disease. In this
scheme, an underlying predisposition for cardiovascular
disease may result in development of both white matter
lesions and preeclampsia without a direct causal relation-
ship between the two. The higher prevalence of current
hypertension in formerly preeclamptic and eclamptic
women is in line with this “stress test” theory and epide-
miologic data. Moreover, the regional distribution of
white matter lesions in these women is similar to what
has been found in other conditions that are associated
with vascular disease such as dementia and migraine.8,9,28
In the elderly, white matter lesions are associated
with stroke, cognitive decline, and dementia.7The
clinical implications of such lesions in our relatively
young cohort of preeclamptic and eclamptic women
are currently unknown. Whether cognitive functioning
may sooner or later also be affected is currently under
investigation. Because a role for posterior reversible
encephalopathy syndrome in the development of white
matter lesions cannot be completely ruled out, also
clinical follow-up of former patients with posterior
reversible encephalopathy syndrome is of interest. In
a rather small percentage of such patients, persistent
neurocognitive complaints and neuroimaging abnor-
malities have been described. Self-perceived cognitive
women.11,12Furthermore, diminished objective neuro-
cognitive functioning, visual disturbances, and epilepsy
have been described after both eclampsia-related as
well as nonobstetric posterior reversible encephalopa-
thy syndrome.14–16,29However, comprehensive longitu-
dinal studies concerning neurocognitive functioning
after posterior reversible encephalopathy syndrome
A few limitations of the current study should be
noted. First, because neuroimaging is not a standard
procedure during preeclampsia and eclampsia, the
location of cerebral edema in the acute phase of
posterior reversible encephalopathy syndrome cannot
be individually related to the distribution of lesions
years later. Furthermore, which preeclamptic women
potentially had posterior reversible encephalopathy
syndrome is not known. Second, white matter lesions
may have been present before the index pregnancy,
but this information is obviously not available. Third,
we might have slightly overestimated the prevalence
of lesions per brain region because it is technically not
feasible to correct for inclusion of partial volume.
This study describes the regional distribution of
white matter lesions in formerly preeclamptic and
eclamptic women as well as parous women who never
regional distribution of white matter lesions, mostly
in the frontal lobe, may be a reflection of the pre-
disposition for vascular disease in formerly eclamptic
and preeclamptic women. The difference in chronic
hypertension incidence between women in the control
group and study patients may explain a major part of
the difference in the presence of subcortical lesions and
future study should explore the role of chronic
hypertension and brain white matter lesions in indi-
viduals in the reproductive age group. Whether
a history of posterior reversible encephalopathy syn-
drome plays an additional role remains speculative but
is less likely. These findings may add to the existing
literature concerning the importance of evaluation of
in formerly eclamptic
Wiegman et al Cerebral Lesions After Preeclampsia and EclampsiaOBSTETRICS & GYNECOLOGY
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