Epilepsy & Behavior 29 (2013) 374378

Contents lists available at ScienceDirect

Epilepsy & Behavior

journal homepage: www.elsevier.com/locate/yebeh

Risks of subsequent epilepsy among patients with hypertensive

encephalopathy: A nationwide population-based study
Tzu-Tsao Chung a,1, Chi-Yu Lin b,1, Wen-Yen Huang c,d, Cheng-Li Lin e,f,
Fung-Chang Sung g,h,i,j, Chia-Hung Kao d,e,
a

Department of Neurological Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan
Department of Neurology, Changhua Christian Hospital, Changhua, Taiwan
Department of Radiation Oncology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan
d
Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan
e
Management Ofce for Health Data, China Medical University Hospital, Taichung, Taiwan
f
Department of Public Health, China Medical University, Taichung, Taiwan
g
Graduate Institute of Clinical Medicine Science, College of Medicine, China Medical University, Taichung, Taiwan
h
School of Medicine, College of Medicine, China Medical University, Taichung, Taiwan
i
Department of Nuclear Medicine, China Medical University Hospital, Taichung, Taiwan
j
PET Center, China Medical University Hospital, Taichung, Taiwan
b
c

a r t i c l e

i n f o

Article history:
Received 15 May 2013
Revised 10 August 2013
Accepted 12 August 2013
Available online 30 September 2013
Keywords:
Hypertensive encephalopathy
Epilepsy
Seizure
Reversible posterior leukoencephalopathy
syndrome
Risk factors

a b s t r a c t
Background: To determine whether the diagnosis of hypertensive encephalopathy (HE) is linked to an increased
risk of subsequent epilepsy by using a nationwide population-based retrospective study.
Methods: Our study featured a study cohort and a comparison cohort. The study cohort consisted of all patients
with newly diagnosed HE between 1997 and 2010, compiled from universal insurance claims data on patients
with hypertension taken from the National Health Insurance Research Database. The comparison cohort
comprised the remaining hypertensive patients without encephalopathy. The follow-up period was terminated
following the development of epilepsy, death, withdrawal from the National Health Insurance system, or the end
of 2010. We determined the cumulative incidences and hazard ratios (HRs) of epilepsy development.
Results: The incidence of subsequent epilepsy was 2.25-fold higher in the patients with HE than in comparisons
(4.17 vs. 1.85 per 1000 person-years), with an adjusted HR of 2.06 (95% CI = 1.662.56) in the multivariable
Cox proportional-hazards regression analysis. The incidence of epilepsy was higher in men, younger patients
with HE, and those with brain disorders.
Conclusions: We found that, in Taiwan, patients with HE are at an increased risk of subsequent epilepsy. Physicians should be aware of HE's link to epilepsy when assessing patients with HE.
2013 Elsevier Inc. All rights reserved.

1. Introduction
In 1928, Oppenheimer et al. rst introduced the term hypertensive
encephalopathy (HE) to describe acute episodes of several cerebral
phenomena correlated with hypertension [1]. It is now known as an
acute organic brain syndrome characterized by unspecic neurological
symptoms such as headache, visual disturbance, altered mental status,
and seizure [2]. The term reversible posterior leukoencephalopathy
syndrome has also been used because the most common abnormality
associated with the syndrome in computed tomography and magnetic

Corresponding author at: Graduate Institute of Clinical Medicine Science and School of
Medicine, China Medical University, 2 Yuh-Der Road Taichung 404, Taiwan. Fax: +886 4
2233 6174.
E-mail address: d10040@mail.cmuh.org.tw (C.-H. Kao).
1
Tzu-Tsao Chung and Chi-Yu Lin contributed equally to this work.
1525-5050/$ see front matter 2013 Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1016/j.yebeh.2013.08.013

resonance images is edema involving white matter in the parietooccipital areas [24]. It is suggested that extreme elevation of systemic
blood pressure causes the breakdown of the autoregulatory capability
of the brain vasculature, resulting in associated neurological syndromes
[4]. Although HE is usually reversible, failure to promptly treat the
dramatic rise in blood pressure may lead to fatal consequences. It is an
emergent syndrome that requires correct identication and early management. The exact incidence of HE is unknown. However, hypertensive
crises represent more than one-fourth of all medical emergencies and
can result in acute end-organ injuries such as cerebral infarction, acute
myocardial infarction, heart failure, acute renal failure, and HE [5].
Epilepsy is commonly concomitant with acute episodes of HE, most
likely because of the irritation caused by transudate in the interstitium.
However, the probability and frequency of epilepsy in the durable
follow-up of patients with a history of acute episodes of HE remain
unclear. The understanding of this issue may provide information valuable to follow-up strategies for patients with HE.

T.-T. Chung et al. / Epilepsy & Behavior 29 (2013) 374378

In this study, we investigated whether the diagnosis of HE is linked

to an increased risk of developing subsequent epilepsy by using the
Taiwanese National Health Insurance Research Database (NHIRD). The
database is available to researchers in Taiwan and has been extensively
used in epidemiologic studies [6]. The wide coverage of this large,
nationwide database allowed us to examine the relationship between
HE and the subsequent development of epilepsy.
2. Materials and methods
2.1. Data sources
This retrospective study used data retrieved from several claims les
of the NHIRD, managed by Taiwan's National Health Insurance Research
Institute (NHRI) at the Department of Health. The universal National
Health Insurance (NHI) program was implemented in March 1995
in Taiwan and covered approximately 99% of the total 23.74-million
residents in 2009. This study analyzed the nationwide populationbased database released by the NHRI from 1996 to 2010 for academic
and administrative use. The NHI database includes information on the
basic patient demographic status, medical institutions, details of inpatient orders, ambulatory care, expenditures for care, and physicians
providing services. To protect patient privacy, all patient-level information can be retrieved and linked only through scrambled personal identication. This study was approved by the Ethics Review Board of China
Medical University (CMU-REC-101-012).
2.2. Study patients
We identied patients with a diagnosis of hypertension (ICD-9-CM
codes 401405) from claims data for inpatients for 19972010. Patients
aged 20 years and older with newly diagnosed HE (ICD-9-CM code
437.2) were selected for the study cohort. The inpatient diagnosis date
was dened as the index date. The comparison cohort was randomly selected from the rest of the hypertensive patients without a history of HE.
For each patient in the study cohort, 4 comparisons were randomly selected, frequency-matched by sex, age (every 5-year span), and the year
of the index date. Patients with any record of epilepsy and/or stroke
(ICD-9-CM codes 430438) before the index date were excluded. In
order to exclude acute provoked seizure, we set a lag time of 1 week
to exclude those who had seizures in the rst week after the diagnosis
of HE. Thus, 5 patients were excluded: 3 in the study cohort and 2 in
the comparison cohort.
2.3. Outcome measures
Both cohorts were followed from the index date to the date the patients received the diagnosis of epilepsy (ICD-9-CM code 345) or until
the patients were censored because of lack of follow-up, death, withdrawal from the NHI system, or the end of 2010. Because epilepsy was
an emergent and critical condition clinically, we believed that physicians made the diagnosis with caution. We supposed that one coding
of 345 was enough to dene the epilepsy. The comorbidities considered
in this study included head injury (ICD-9-CM codes 850854, 959.01),
meningitis (ICD-9-CM codes 0130, 0360,0470, 0471, 0478, 0479, 0490,
0491, 0530, 0721, 0942, 1142, 320, 321, 322, 00321, 05472, 09042,
09181, 09882, 10081, 11283, 11501, 11591), encephalitis (ICD-9-CM
codes 0136, 0361, 0462, 0520, 0550, 0722, 1390, V050, 062, 063, 064,
323, 09041, 09481), multiple sclerosis (ICD-9-CM code 340), and alcoholism (ICD-9-CM codes 303, 305.00, 305.01, 305.02, 305.03, V11.3).
2.4. Statistical analysis
The sociodemographic distribution and prevalence of comorbidities
were compared between the study and comparison cohorts and examined using the 2 test. The sex-, age-, and comorbidity-specic incidence

375

densities of epilepsy were measured and compared for both cohorts.

Poisson regression was used to estimate an incidence rate ratio (IRR)
and a 95% condence interval between the study cohort and the
comparison cohort. Multivariate Cox proportional-hazards regression
analysis was used to estimate the risk of epilepsy in association
with HE, controlling for sociodemographic factors and comorbidities.
The follow-up years were partitioned into 4 segments (3 years,
36 years, 69 years, and N 9 years) to observe the change in epilepsy
hazard. The cumulative incidence of epilepsy for both the study
and the comparison cohorts was calculated using the KaplanMeier
method, and the difference was tested using the log-rank test. The
analyses were performed using the SAS statistical package (version
9.2; SAS Institute Inc., Cary, NC, USA), and the KaplanMeier survival
curve was plotted using R software (R Foundation for Statistical
Computing, Vienna, Austria). The statistical signicance was accepted
at an -value of 0.05.
3. Results
Among patients with hypertension but free from stroke, we identied
5766 patients with HE for the study cohort and selected 23,074 patients
for the comparison cohort. Patients in both cohorts were predominantly
female and over 65 years of age. Comorbidities were more prevalent
in the study cohort than in the comparison cohort, particularly for head
injury, meningitis, encephalitis, and alcoholism (Table 1).
The incidence of epilepsy in the study cohort was 2.26-fold greater
than that in the comparison cohort (4.17 vs. 1.85 per 1000 personyears), with an adjusted HR of 2.06 (95% CI: 1.662.56) (Table 2). Men
were at higher risk than women to have epilepsy in both cohorts. The
HE to non-HE adjusted HR was also higher for males than for females
(2.27 vs. 1.84). Age-specic data showed that epilepsy incidence was
the highest in patients with HE 2039 years of age, although there
were more cases of epilepsy in the older groups. The study cohort to
comparison cohort relative risk of epilepsy was the highest for those
aged 4064 years old, with an adjusted HR of 2.59 (p b 0.001).
Table 2 also shows that epilepsy incidence increased for those with comorbidity, with the highest incidence for those with meningitis,
followed by those with encephalitis, alcoholism, and head injury.
The incidence of epilepsy was consistently higher in the study cohort
with HE than in the comparison cohort during the follow-up period
(Table 3). The incidence of epilepsy was the highest during the initial
3 years after HE diagnosis with an adjusted HR of 3.03 compared with
the corresponding comparisons. The cumulative incidence curve for
Table 1
Demographic characteristics and comorbidity in patients with and without hypertensive
encephalopathy.
Variable

Sex
Female
Male
Age, median (IQR)
Stratied age
2039
4064
65+
Comorbidity
Head injury
Meningitis
Encephalitis
Multiple sclerosis
Alcoholism
a
b

Chi-square test.
MannWhitney U test.

Hypertensive encephalopathy

p-Valuea

No

Yes

N = 23,074

N = 5766

n (%)

n (%)

13,210 (57.3)
9864 (42.8)
69.5 (59.177.0)

3303 (57.3)
2463 (42.7)
69.5 (59.176.9)

648 (2.81)
8024 (34.8)
14,402 (62.4)

161 (2.79)
2004 (34.8)
3601 (62.4)

0.99

2541 (11.0)
103 (0.45)
48 (0.21)
8 (0.03)
232 (1.01)

1190 (20.6)
49 (0.85)
22 (0.38)
2 (0.03)
84 (1.46)

b0.0001
0.0002
0.02
0.30
0.003

0.99
0.84b

376

T.-T. Chung et al. / Epilepsy & Behavior 29 (2013) 374378

Table 2
Incidence of epilepsy by sex, age, and comorbidity and Cox model-measured hazards between patients with and without hypertensive encephalopathy.
Hypertensive encephalopathy
No
Variables
c

All
Sexd
Female
Male
Stratied agee
2039
4064
65+
Comorbidity
Head injuryf
No
Yes
Meningitisg
No
Yes
Encephalitish
No
Yes
Multiple sclerosisi
No
Yes
Alcoholismj
No
Yes

Yes
a

IRRb (95% CI)

Adjusted HR (95% CI)

4.17

2.26 (2.08, 2.44)

2.06 (1.66, 2.56)

16,939
11,574

3.13
5.70

1.94 (1.74, 2.17)

2.61 (2.33, 2.94)

1.84 (1.34, 2.53)

2.27 (1.69, 3.07)

5
45
69

920
12,049
15,545

5.43
3.73
4.44

1.89 (1.21, 2.96)

2.98 (2.62, 3.40)
1.99 (1.79, 2.20)

1.58 (0.54, 4.61)

2.59 (1.78, 3.76)
1.83 (1.38, 2.42)

1.54
4.21

87
32

22,414
6100

3.88
5.25

2.52 (2.31, 2.75)

1.25 (1.02, 1.53)

2.55 (1.98, 3.27)

1.23 (0.81, 1.87)

155,051
613

1.81
11.4

113
6

28,285
228

4.00
26.3

2.20 (2.03, 2.39)

2.30 (1.07, 4.97)

2.06 (1.65, 2.57)

2.00 (0.59, 6.80)

286
2

155,309
356

1.84
5.62

118
1

28,437
76

4.15
13.2

2.25 (2.08, 2.44)

2.33 (0.57, 9.51)

2.05 (1.64, 2.55)

2.21 (0.14, 34.7)

288
0

155,597
67

1.85
0.00

119
0

28,511
2.74

4.17
0.00

2.26 (2.08, 2.44)

2.06 (1.66, 2.56)

279
9

154,099
1566

1.81
5.75

116
3

28,039
474

4.14
6.33

2.29 (2.11, 2.48)

1.10 (0.56, 2.18)

2.10 (1.68, 2.62)

1.06 (0.28, 4.00)

Event

PY

1.85

119

28,513

89,951
65,713

1.61
2.18

53
66

13
80
195

4526
63,902
87,236

2.87
1.25
2.24

212
76

137,599
18,065

281
7

Event

PY

288

155,664

145
143

Rate

Ratea

Incidence rate per 1000 person-years.

Incidence rate ratio.
c
Adjusted HR was calculated by Cox proportional hazard regression and adjusted for age, sex, head injury, meningitis, encephalitis, and alcoholism.
d
Adjusted HR was calculated by Cox proportional hazard regression stratied by sex and adjusted for age, head injury, meningitis, encephalitis, and alcoholism.
e
Adjusted HR was calculated by Cox proportional hazard regression stratied by age and adjusted for sex, head injury, meningitis, encephalitis, and alcoholism.
f
Adjusted HR was calculated by Cox proportional hazard regression stratied by head injury and adjusted for age, sex, meningitis, encephalitis, and alcoholism.
g
Adjusted HR was calculated by Cox proportional hazard regression stratied by meningitis and adjusted for age, sex, head injury, encephalitis, and alcoholism.
h
Adjusted HR was calculated by Cox proportional hazard regression stratied by encephalitis and adjusted for age, sex, head injury, meningitis, and alcoholism.
i
Adjusted HR was calculated by Cox proportional hazard regression stratied by multiple sclerosis and adjusted for age, sex, head injury, meningitis, encephalitis, and alcoholism.
j
Adjusted HR was calculated by Cox proportional hazard regression stratied by alcoholism and adjusted for age, sex, head injury, meningitis, and encephalitis.
p b 0.05.
p b 0.01.
p b 0.001.
b

epilepsy showed that the study cohort had a signicantly higher risk of
epilepsy than the comparison cohort (log-rank test b 0.0001) (Fig. 1).
4. Discussion
To the best of our knowledge, this study is the rst attempt to investigate the risk of epilepsy among patients with HE after adjusting for
patient comorbid medical disorders by using a nationwide populationbased data set. Our study shows that the likelihood of epilepsy development is 2.06-fold greater among patients with HE than among hypertensive patients without encephalopathy. Furthermore, we found that
patients with HE with comorbidities of head injury, meningitis, and

alcoholism were at an additionally higher risk of epilepsy than those

without the comorbidities.
The overall demographic-specic incidence of epilepsy after stratied analyses of sex and age is signicantly higher in the cohort with
HE than in the comparison cohort. We found that the relative risk of
epilepsy was higher in men than in women (adjusted HR = 2.27 vs.
1.84), concurring with well-established databases of sex comparisons
in epilepsy [7].
Moreover, the relative incidence of epilepsy is still higher in the
long-term follow-up, further conrming that the risk of epilepsy in
patients with HE is truly increased. Furthermore, approximately half
of epilepsy diagnoses occurred within the initial 3 years after the rst

Table 3
Hazard ratio for epilepsy compared between patients with and without hypertensive encephalopathy by follow-up duration.
Hypertensive encephalopathy
Follow-up timea

3 years
36 years
69 years
N9 years
a

No

Yes
b

IRRc (95% CI)

Adjusted HR (95% CI)

3.23 (2.98, 3.51)

1.82 (1.63, 2.02)
1.72 (1.51, 1.96)
1.95 (1.63, 2.32)

3.03 (2.17, 4.23)

1.65 (1.08, 2.52)
1.48 (0.90, 2.45)
1.57 (0.78, 3.17)

Event

PY

Rate

Event

PY

Rate

88
89
72
39

61,247
46,898
30,892
16,625

1.44
1.90
2.33
2.35

59
29
20
11

12,699
8414
4990
2410

4.65
3.45
4.01
4.56

Adjusted HR was calculated by Cox proportional hazard regression stratied by follow-up duration and adjusted for age, sex, head injury, meningitis, encephalitis, and alcoholism.
Incidence rate per 1000 person-years.
Incidence rate ratio.
p b 0.05.
p b 0.01.
p b 0.001.
b
c

T.-T. Chung et al. / Epilepsy & Behavior 29 (2013) 374378

Fig. 1. Cumulative incidence of epilepsy compared between cohorts with and without
hypertensive encephalopathy using the KaplanMeier method.

377

6 months, 50% within 1 year, and 80% within 2 years [17,18]. The
more severe the head injury, the longer the patient is at risk for late seizures. This information has implications in the follow-up strategy and
management of patients with HE.
A particular strength of this study is the use of a nationwide
population-based data set that provides a sufcient sample size and statistical power to explore the link between HE and epilepsy. In addition,
the patients in our study displayed a wide range of demographic characteristics, which allowed us to perform stratied analyses according to
sex, age, and comorbidities. Nevertheless, some insufciencies in our
study should be addressed. First, additional theoretically relevant confounding variables such as smoking, diabetes, and a family history of
epilepsy could not be included in our analysis because they were not included in our data set. Further study is needed to clarify the effects
of these factors. Second, we might not be able to completely exclude
study subject misclassication. A patient with HE, with symptoms of
headache, visual disturbance, and altered mental status but no seizure,
might not seek medical advice and may thus be misclassied as having
hypertension only and be included in the comparison cohort. We believed that this probability was extremely low because few patients
would tolerate acute HE symptoms without medical intervention.
Moreover, our patients could seek medical advice easily because of the
high accessibility of medical services in Taiwan.
5. Conclusion

episode of HE, with a decreased relative incidence of epilepsy in the

prolonged follow-up. In a recent meta-analysis, the estimated median
incidence of epilepsy was 0.504 per 1000 person-years [8]. However,
the overall incidence of epilepsy in our study was high, with a rate
of 4.17 per 1000 person-years in the cohort with HE and 1.85 per
1000 person-years in the comparison cohort. This is probably because
the participants were relatively older; 62.4% of both cohorts were age
65 or older. However, the age-specic incidence of epilepsy was the
lowest for those aged 4064, indicating a U-shape association with
age. With the highest incidence of epilepsy, younger patients with HE
deserve greater attention after the diagnosis of HE.
Changes in the degree of hypertension can generate the autoregulatory dysfunction of cerebral blood ow [9]. Recent reports assert
that HE occurs in 15%20% of patients in whom malignant hypertension
was present [10,11]. It is an acute organic brain syndrome resulting
from disrupted autoregulation of cerebral blood ow. An acute provoked seizure is a frequently concomitant with HE [2,12]. There may
be generalized, focal, or focal with secondarily generalized tonicclonic
convulsions. The pathogenesis of acute provoked seizure following HE
is incompletely understood. It seems to be the irritative effects of the
uid in the brain interstitium related to cytotoxic edema or vasogenic
edema [1,3,1315]. The cytotoxic edema results from the infarction
caused by thrombosis of arterioles and brinoid necrosis [1315].
Conversely, vasogenic edema is related to hypertensive cerebrovascular
endothelial dysfunction or disruption of the bloodbrain barrier with
increased permeability [3,9,15]. However, the disruption is the most
widely accepted basis for HE [16]. Therefore, to reduce acute provoked
seizure, neuroprotection following diagnosis of HE deserves further research. The pathogenesis of later spontaneous unprovoked seizures, the
endpoint of the present study, is even less studied and discussed. It may
reect more permanent structural and physiologic changes within the
brain. We found an increased risk of later epilepsy in patients with HE.
This may provide the basis of ongoing research on the pathogenesis
and prevention strategy of later spontaneous unprovoked seizures in
patients with HE.
The timing of the most development of spontaneous unprovoked
seizures after HE is important. We found that most of the seizures happened in the rst 3 years even though the increased incidence of epilepsy was found within 6 years after occurence of HE. This pattern is
similar to that of epilepsy after a traumatic brain injury. Approximately
40% of individuals with epilepsy after head trauma have onset within

We found that the risk for epilepsy in Taiwan was approximately

2.24-fold greater among patients who had been previously diagnosed
with HE compared to those who had not and that this association was
entirely independent of age, sex, head injury, meningitis, encephalitis,
alcoholism, and multiple sclerosis. Thus, physicians should be aware
of HE's link to epilepsy when assessing patients with HE. Furthermore,
because approximately half of the epilepsy diagnoses occurred within
3 years from the onset of HE, routine follow-up examinations and control of blood pressure should be performed for at least 3 years.
Contributors
Conception/design: Tzu-Tsao Chung, Chi-Yu Lin, and Chia-Hung Kao.
Provision of study material or patients: Wen-Yen Huang, Cheng-Li
Lin, and Fung-Chang Sung.
Collection and/or assembly of data: Cheng-Li Lin and Fung-Chang
Sung.
Data analysis and interpretation: Tzu-Tsao Chung, Chi-Yu Lin,
Wen-Yen Huang, Fung-Chang Sung, and Chia-Hung Kao.
Manuscript writing: All authors.
Final approval of manuscript: All authors.
Conict of interest
All authors state that they have no conicts of interest.
Acknowledgments
The study was supported in part by the study projects (DMR-101061 and DMR-100-076) in China Medical University hospital, the
Taiwan Department of Health Clinical Trial and Research Center and
for Excellence (DOH102-TD-B-111-004), and the Taiwan Department
of Health Cancer Research Center for Excellence (DOH102-TD-C-111005). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
References
[1] Oppenheimer BS, Fishberg AM. Hypertensive encephalopathy. Arch Intern Med
(Chic) 1928;41:26478.

378

T.-T. Chung et al. / Epilepsy & Behavior 29 (2013) 374378

[2] Weingarten KL, Zimmerman RD, Pinto RS, Whelan MA. Computed tomographic
changes of hypertensive encephalopathy. AJNR Am J Neuroradiol 1985;6:3958.
[3] Schwartz RB, Jones KM, Kalina P, Bajakian RL, Mantello MT, Garada B, et al. Hypertensive encephalopathy: ndings on CT, MR imaging, and SPECT imaging in 14
cases. AJR Am J Roentgenol 1992;159:37983.
[4] Hinchey J, Chaves C, Appignani B, Breen J, Pao L, Wang A, et al. A reversible posterior
leukoencephalopathy syndrome. N Engl J Med 1996;334:494500.
[5] Papadopoulos DP, Mourouzis I, Thomopoulos C, Makris T, Papademetriou V. Hypertension crisis. Blood Press 2010;19:32836.
[6] Chen YC, Wu JC, Chen TJ, Wetter T. Reduced access to database. A publicly available
database accelerates academic production. BMJ 2011;342:d637.
[7] McHugh JC, Delanty N. Epidemiology and classication of epilepsy: gender comparisons. Int Rev Neurobiol 2008;83:1126.
[8] Ngugi AK, Kariuki SM, Bottomley C, Kleinschmidt I, Sander JW, Newton CR. Incidence
of epilepsy: a systematic review and meta-analysis. Neurology 2011;77:100512.
[9] Vaughan CJ, Delanty N. Hypertensive emergencies. Lancet 2000;356:4117.
[10] Amraoui F, van Montfrans GA, van den Born BJ. Value of retinal examination in
hypertensive encephalopathy. J Hum Hypertens 2010;24:2749.

[11] Zampaglione B, Pascale C, Marchisio M, Cavallo-Perin P. Hypertensive urgencies and emergencies. Prevalence and clinical presentation. Hypertension
1996;27:1447.
[12] Delanty N, Vaughan CJ, French JA. Medical causes of seizures. Lancet 1998;352:38390.
[13] Weingarten K, Barbut D, Filippi C, Zimmerman RD. Acute hypertensive encephalopathy: ndings on spin-echo and gradient-echo MR imaging. AJR Am J Roentgenol
1994;162:66570.
[14] Chester EM, Agamanolis DP, Banker BQ, Victor M. Hypertensive encephalopathy: a
clinicopathologic study of 20 cases. Neurology 1978;28:92839.
[15] Schaefer PW, Buonanno FS, Gonzalez RG, Schwamm LH. Diffusion-weighted imaging
discriminates between cytotoxic and vasogenic edema in a patient with eclampsia.
Stroke 1997;28:10825.
[16] Bhagavati S, Chum F, Choi J. Hypertensive encephalopathy presenting with isolated
brain stem and cerebellar edema. J Neuroimaging 2008;18:4546.
[17] Annegers JF, Grabow JD, Groover RV, Laws Jr ER, Elveback LR, Kurland LT. Seizures
after head trauma: a population study. Neurology 1980;30:6839.
[18] Annegers JF, Hauser WA, Coan SP, Rocca WA. A population-based study of seizures
after traumatic brain injuries. N Engl J Med 1998;338:204.