1 Neurological Department Faculty of Medicine ULM, Banjarmasin

Fakhrurrazy et al

Case Report*

CLINICAL AND RADIOLOGICAL APPROACH OF POSTERIOR

REVERSIBLE ENCEPHALOPATHY SYNDROME ON ECLAMPSIA
Fakhrurrazy**, Herly*.
**Lecturer, neurological department faculty of medicine Lambung Mangkurat University, Banjarmasin.
*Young doctor, neurological department faculty of medicine Lambung Mangkurat University, Banjarmasin.

Introduction. Posterior reversible encephalopathy syndrome (PRES) is rare cliniconeuroradiologic condition and not commonly reported in the literature, a recently recognized
syndrome characterized, clinically by headache, confusion, seizure and visual loss associated
with imaging findings of bilateral cortical and subcortical oedema, predominantly posterior
cerebral lesions (mainly occipito-parietal). Posterior reversible encephalopathy syndrome is an
uncommon complication of severe preeclampsia/ eclampsia.
Aim. To report PRES case on eclampsia with clinical and radiological approach.
Case Report. Women, 34 years old, with chief complaint tonic clonic general seizure and
sudden headache previously. This patient had pregnancy 8 gestational month and had pregnancy
termination with cesarean section recently. Patient is having loss of consciousness, vision
disturbance, and weakness right extremities, all this symptom become well during treatment. The
result of laboratory examination is HELLP syndrome (haemolysis, elevated liver enzymes and
low-platelets). Head CT scan show hypodense lesion in left parietooccipital region and MRI on
T2W and T2FLAIR ADC MAPPS found hyperdens lesion in right and left parietooccipital.
Conclusion. It have been reported cases of eclampsia with PRES with symptom of headache,
seizure, mental status disturbance, visual disturbances. The pathological association between
PRES and HELLP syndrome in a patient with eclampsia is poorly described.
Key Words: posterior reversible encephalopathy syndrome, clinical, radiological, eclampsia.
Introduction
Posterior

increased blood pressure or any

reversible

particular drug consumption (1,2).

encephalopathy syndrome (PRES) is

Imaging

modality

a syndrome that clinically present

symmetrical

with headache, confuse, seizure,

substantia

alba

and visual loss. Since the first

grisea.

proper

description in 1996, PRES has been

treatment

reported to be formed in central

particular drug becomes important

clinical

in order to assure reversibility of

condition,

weither

with

the

deficit.

lesion

showed

or

usually

and

posterior

hypertension

not

This

at

using

following

any

case

2 Neurological Department Faculty of Medicine ULM, Banjarmasin

Fakhrurrazy et al

report

was

reported

about

The physical examination at

eclampsia case that develop into

the first time came to hospital was

PRES (3).

somnolence (induced by diazepam),

The pathophysiology of this

blood

pressure

120/80

mmHg,

disease is not fully understood yet.

axillary temperature 36.5 0C, heart

It is happen to be multifactorial with

rate 106/ minute, respiratory rate

the result in vasogenic edema of

20/ minute , height 155 cm, and

brain

weight

tissue,

combination

of

65

kg.

Thorax

and

vasogenic-sitotoxic edema (4).

abdominal examination was normal,

Case Report

lower

extremity

edema,

and

A 34-year-old woman came

another systemic examination was

with a general tonic clonic seizure

normal. Neurological examination

as the main complaint. The patient

shown visual acuity OD and OS

had a sudden severe headache

2/60,

before the seizure, the headache

babinski reflex was found.

dexter

was felt around the head. She had

been

having

eight

month

hemiparesis,

right

Laboratorium results was

increasing

of

transaminase

liver

pregnancy at that time and it was

enzyme, SGOT 396 U/L (normal: 11-

her fifth pregnancy. At the day three

39 U/L) and SGPT 376 U/L (normal :

of

10-37

care

her

pregnancy

were

U/L);

urea

creatinine

the day four of care the patient was

cholesterol 271, triglycerides 371,

apathetic and got an imaging of

albumin

right lateralization, and at the day

hemoglobin

five she was compos mentis and

g/dL), leukosit 14.09/mm3 (4.000-

weakness of the right limb, burred

11.000

vision, and the patient

21.000

2.3,

hematokrit

8.7

mm3)
/mm3

mg/dL,

mg/dL,

terminated by sectio caesarea. At

could only

0.59

64

g/dL

total
26.1%,

(12.3-15.3

and

platelet

(150.000-450.000

see a hand motion from a half

mm3). A routine urine result was

meter in both of eyes. After a few

proteinuria.

days, the viusal acuity and the right

supported HELLP syndrome.

limb weakness was better.

These

findings

3 Neurological Department Faculty of Medicine ULM, Banjarmasin

Fakhrurrazy et al

Head CT scan results with and

contrast.

without contrast shown hypodens

lesion at parietooccipital sinister
with

oedem

perifocal

enhancement

with

the

and

soft

contrast.

Cranial MRI T1W with and without

contrast, T2W and T2FLAIR ADC
MAPPS, shownl hyperdens lesion at
T2W and T2FLAIR ADC MAPPS at
right

and

left

parietooccipital

unclear at T1W and no presenting

of

enhancement

post

contrast

(image below).

Fig (2). Axial Head CT scan with

contrast.

Fi

Fig (3). Transversal Head MRI T1W1.

g (1). Axial Head CT scan without

Fig (4). Transversal Head MRI T2.

4 Neurological Department Faculty of Medicine ULM, Banjarmasin

Fakhrurrazy et al

signs and radiological disorder of

occipital alba substancia, usually
bilateral,

marked

by

cerebral

edema with hipodens sign at CT

scan and hiperdens sign at T2
Fig (5). Transversal Head MRI T2
FLAIR.

weighted

by

MRI

imaging.

This

syndrome occurs on the patient

that

has

encephalopathy

hypertension,

renal

failure,

immunosuppression,

and

postpartum eclampsia (4).

Seizures

are

cited

as

the

commonest manifestation of PRES,

occurring in up to 90% of reported

Fig (6). Head MRI ADC MAPS

cases. Seizure activity on the EEG

Discussion
Posterior

reversible

was

defined

as

continuous

encephalopathy syndrome (PRES),

recurrent

as

generalized spikes; sharp waves;

constellation of symptoms caused

spike waves; or rhythmic waves

by

most

changing in amplitude, frequency,

commonly of the posterior cerebral

and/ or spatial distribution. Visual

vasculature,

disturbances

the

name

reversible

suggests,
ischemia

thus

affecting

is

the

complaints

parietal- occipital region (5).

Posterior

reversible

encephalopathy

syndrome

rhythmic

firstly

cortical

can
of

focal

or

range

blurred

blindness.

or

from

vision

to

Symptoms

develop over hours and can persist

explained by Hinchey et al. at 1996

for

and

severity and the latency in initiating

well

posterior

known

as

reversible

leucoencephalopathy

weeks,

proper

depending
treatment.

on

the
Acute

syndrome too, the clinical definition

hypertension is also associated with

is an association of neurological

the majority of PRES cases, but is

not necessary for the diagnosis,

5 Neurological Department Faculty of Medicine ULM, Banjarmasin

Fakhrurrazy et al

and the degree of elevation varies

image

(6,7).

substantia alba subcortical (11).

Eclampsia

is

serious

at

posterior

cortex

and

The mecanism the posterior

complication that occurs at 5% of

dominant

pregnancy

of

considered to be related to a sparse

mortality.

distribution of symphatetic nerve in

Clinical eclampsia is defined as

the vertebra basilar circulation, in

seizure or coma that related with

contrast to the anterior cerebral

gestational

circulation,

and

causes

gestational-related

and

10%

induced

by

involvement

which

is

is

richly

hypertension. The patient is usually

innervated by symphatetic nerve

followed by headache, change of

(12). Several proposed mechanisms

mental status, cortical blindness,

include

and

autoregulation

seizure

(8).

Eclampsia

and

disruption

cerebral

during periods

high

In addition, the fluctuation of blood

incompetency of the blood-brain

pressure can causes various degree

barrier

of vasospasm and vasodilatation. At

endothelial dysfunction leading to

the end, cerebral autoregulation

disruption

of

disorder causes disruption of blood

integrity;

and

brain barrier at posterior circulation

vasospasm

(9,10).

angiography. Clinically, symptoms

eclampsia

is

identic

hypertension encephalopathy.
scan

shows

posterior

is

better

than

vasogenic

edema;

blood-brain
focal

seen

on

to

barrier

or

diffuse
catheter

with

have a wide range of presentations

Ct

depending on the area of the brain

transitorik
CT

and

leading

develop acutely over hours and can

involved (13).

area shows patchy low attenuation.

MRI

pressure

of

other pathological can cause PRES.

The imaging of patient with

blood

of

The

brain

perfusion

is

on

defended by autoregulatic system

encephalopathy eclampsia imaging.

of small artery and arteriola that

The lesion is marked by a low

have

intensity sign on T1-weighted and

components.

high intensity sign on T2-weighted

endothel may attenuate or obviate

myogenic

and

neurogenic

Destruction

of

6 Neurological Department Faculty of Medicine ULM, Banjarmasin

Fakhrurrazy et al

the myogenic respond. Perivascular

can

sympathetic nerve, that will protect

seizure (17,18).

the brain if myogenic respond does

not

respond

founded

on

or

over

adventitial

be

represented

edema

Computed tomography (CT)

respond,

scan shown

layer

particularly

of

by

vasogenic edema,
at

substantia

alba

subcortical,

yet

brains vessels and protected from

parietooccipital

endothel destroyer agent. Thus the

brain stem area, cerebellum, frontal

vertebrobasilar system and cerebral

lobe, and ganglia basale could be

posterior

be

involved (19). The new findings on

innervated by sympathetic nerve,

Magnetic Resonance Imaging (MRI)

systemic pressure (14,15).

and

artery

Recently,
used

USG

is

rare

to

research

doppler

recovery

attenuated
(FLAIR)

inversion

sequences,

shown

diffusion-weighted imaging (DWI),

enhancement of cerebral perfusion

and apparent diffusion coefficient

pressure and lower resistance of

(ADC) mapping shown that edema

cerebrovascular

with

occurred at the both substantia

eclampsia (16), the enhancement

alba and grisea. The etiology of

of blood flow to occipital lobe of the

PRES was still unknown, yet the two

brain at the patient that had SPECT

main

and xenon computed tomography.

proposed about mechanism of the

The seizure more common occurred

course. One of them had opinion

at the patient with brain edema

that autoregulation cerebral failure

compared by the normal one. This

was

finding most likely reflects irritation

Autoregulation

effect of fluid in subcortical and

caused

cortical tissue. Some writers has

enhanced

suggested, based on the correlation

pressure

between

edema (20). The involvement of

at

general

has

that

fluid

patient

seizure

with

theories

that

triggered

by

had

hypertension.

cerebral

vasodilatation
capilary
that
lobe

failure

and

then

hidrostatic

caused
and

been

vasogenic

encephalopathy hypertension, that

parietal

radiography imaging at the patient

considered

with encephalopathy hypertension

innervation of sympathetic nerve

had

occipital

was

relation

with

7 Neurological Department Faculty of Medicine ULM, Banjarmasin

Fakhrurrazy et al

on

posterior

circulation

that

on T2W and FLAIR (8). At this case,

relatively bad. One of the syndrome

DWI, included ADC quantification, is

feature was edema without infark.

the primary imaging modality. This

Thus, introduction and appropriate

new MR shown the movement of

medication of the syndrome was

water molecule used 2 metrics,

very

the

mean diffusivity (MD) and fractional

progressiveness, found and coped

anisotropy (FA), that represented

the

the magnitude and the direction of

important

to

causes

stop

and

prevented

permanent damage or death (21).

water. Cytotoxic edema was caused

Based on the two theories

above,

it

was

determine

important

between

edema

and

cytotoxic

caused

by

different

to

by acute ischemic and infarc, and

gradually

lower

ADC

through

vasogenic

reduction of proton diffusibility. The

edema,

fact above made a brighter sign of

strategy

DWI and was believed reflected

management. suggested to divide

enhancement

the

two

activity and lower extracellular fluid

with

due lower Na+ and K+-ATPase. Yet,

hypertension encephalopathy and

on DWI, vasogenic edema can be

patient with toxic encephalopathy.

looked as enhancement intensity

On

sign

PRES

patient

subgroups,

the

into

patient

patient

with

vasogenic

edema, lowered blood pressure and

(T2

of

intracellular

shine-through

effect)

(22,23).

supporting steps was the first line

The change of MRI of PRES

of treatment, while the patient with

had proved occur on an area that

cytotoxic edema and infark needed

passed by posterior circulation, and

more

disorder

aggressive

approach

that

of

anterior

circulation

followed by another ethiology, such

occurred on severe case. It could be

as

caused by inadequate innervation

subarachnoid

bleeding

with

vasospasme (20).

of

The previous neuroimaging

finding

reported

reversible

hypodens CT and hypersensitivity

sympathetic

vertebrobacilar
cerebral

rather

nerve

artery
than

anterior vessel (24,25).

on

posterior
cerebral

8 Neurological Department Faculty of Medicine ULM, Banjarmasin

Fakhrurrazy et al

The management combined

symptomatic

Posterior

syndrome

life-supporting

encephalopathy reversible was a

treatments and control of the factor

case that needed an immediate

causing PRES. Efforts were made to

therapy, a delay in case might

control systemic secondary brain

caused permanent brain damage.

insults

The PRES therapy involved lowering

and

to

limit

effects

potential

of

cranial

hypertensionhypoglycemia

blood

pressure,

relieved

the

was

predisposition agent, and use of

routinely checked and corrected. If

anticonvulsan drug on patient with

glucose was given, 100 mg of

seizure.

thiamine

disappeared after the therapy and

was

administered

The

seizure

usually

concomitantly, most notably when

not needed furthermore (26).

there was evidence of vitamin B1

Conclusion

deficiency.

Patients

alsoroutinely

The pathophysiology of PRES

for

on patient with eclampsia was did

hyperglycemia,

not known fully. It was believed

evaluated

hyperthermia,
hypo-

were

or

hyper-carbia,

anemia,

came

from

metabolic

disturbances,

epileptic

posterior

vasculopathy

circulation

by

activity and aspiration pneumonia

lower

that

initial

and enhanced by endhotelial cell

consciousness disorders and which

damage. MRI is the best choice of

required prompt correction. Patients

modality, not only to eliminate the

with

different

may

complicate

status

the

epilepticus

were

autoregulation

caused

of

adrenergik

diagnosis,

like

managed as previously described.

encephalitis, trombosis sinus, and

Control of severe hypertension, if

brain

present, was an important part of

particularly ADC quantification, for

the

furthemore

symptomatic

management.

ischemic,
can

but
differ

DWI

and

vasogenic

Intravenous antihypertensive drugs

edema and cytotoxic edema. It was

including labetolol, nicardipine, or

important to differ encephalopathy

urapidil were given (7).

hypertension

and

toxic

encephalopathy, particularly on the

9 Neurological Department Faculty of Medicine ULM, Banjarmasin

Fakhrurrazy et al

patient

specific

encephalopathy syndrome. Am J

symptoms such headache, seizure,

Neuroradiol;29:447-455.
5. Hedna VS, Stead LG, Bidari S,

visual

that

shown

deficit,

and

change

of

mental, it needed to do immediate

medication

to

maximize

Patel A, Gottipati A, Favilla CG.

2012.

Posterior

encephalopathy

reversibility potential.

(PRES)

1. Hong S, Jung JM, Ryu HJ, Kwon

DY, Park MH. 2013. Posterior
Syndrome

Encephalopathy
Following

Rapid

Correction of Anemia. Depart of

Neuro & Dermato; 18(4) : 423.
2. Doelken, M., Lanz S., Rennert J.,
Alibek S., Richter G., Doerfler A.
2007.

Differentiation

of

cytotoxic and vasogenic edema

in

patient

posterior
syndrome
weighted

with

reversible

leukoencephalopathy
using
MRI.

diffusion-

Diagn

Interv

Radiol;13:125-128.
3. Lamy, C., Oppenheim C., Meder
J.F., Mas J.L. 2004. Neuroimaging
in

posterior

encephalopathy

reversible
syndrome.

Neuroimaging; 14:8996.
4. Bartynski, W.S., Boardman J.F.
2008. Catheter angiography, MR
angiography, and MR perfusion
in

posterior

syndrome

and

CT

perfusion

changes. Int Journ of Emergency

REFERENCES

Reversible

reversible

reversible

Med; 5(12):1-3.
6. Graham BR, Pylypchuk
2014.

Posterior

GB.

reversible

encephalopathy syndrome in an
adult

patient

undergoing

peritoneal dialysis: a case report

and

literature

review.

BMC

Nephrology ; 15(10):1-3.
7. Legriel S, Schraub o , Azoulay E,
Hantson P, Magalhaes E, Coquet
I.

2012.

Determinants

of

Recovery from Severe Posterior

Reversible

Encephalopathy

Syndrome.

Medical-Surgical

Intensive Care Department;7(9):

4.
8. Hinchey,

J.,

Chaves

C.,

Appignani B.. 1996. A reversible

posterior

leukoencephalopathy

syndrome.

Engl

Med;

334:494500.
9. Donaldson, J.O. 1988. Eclamptic
hypertensive

encephalopathy.

Semin Neurol;8(3):230233.

10 Neurological Department Faculty of Medicine ULM, Banjarmasin

Fakhrurrazy et al

10.

Schwartz, R.B., Feske S.K.,

14.

Kaskel,

F.J.,

Deverajan

P.,

Polak J.F. 2000. Preeclampsia-

Birzgalis A., Moore L.C. 1989.

eclampsia:

Inhibition

clinical

neuroradiographic
and

correlates

insights

pathogenesis

and

into

of

of

myogenic

autoregulation in cyclosporine

the

nephrotoxicity in the rat. Ren

hypertensive

Physiol Biochem;12:250-259.
15. Williams, K.P., Wilson S. 1999.

encephalopathy.
Radiology;217(2):371376.
11. Sheth,
R.D.,
Riggs
J.E.,

Persistence

of

cerebral

hemodynamic

changes

Bodenstenier J.B., Gutierrez A.R.,

patients

eclampsia:

Ketonen L.M., Ortiz O.A. 1996.

report of three cases. Am J

Parietal

Obstet

occipital

edema

in

hypertensive encephalopathy: a
pathogenic

mechanism.

Eur

Neurol;36(1):2528.
12. Hata M, Oishi A, Kurimoto Y,
Yamamoto S, Kohara N. 2011. A
Case

of

Posterior

Encephalopathy
Presenting
Diplopia.

Reversible
Syndrome

With
J

Vlinic

Isolated
Experiment

Ophtalmo;2(5):2.
13. Cai X, Bhattacharyya S, Plitt
A, Raibagkar P, LaBuzetta ZN.
Schleicher

SM.

2014.

Management

of

Reversible

Encephalopathy

Syndrome

Posterior

Induced

by

Carfilzomib in a Patient With

Multiple

Myeloma.

Clinical Onco;32:4.

Journ

of

with

Gynecol;

1165.
16. Ohnom,

Y.,

in
a

181:1162

Wakahara

Y.,

Kawai M., Arii Y. 1999. Cerebral

hyperperfusion in patient with
eclampsia. Acta Obstet Gynecol
Scand; 78:555556.
17. Yaffe,
K.,
Ferriero

D.,

Barkovich A.J., Rowley H. 1995.

Reversible

MRI

abnormalities

following Seizures. Neurology;

45:104108
18. Puppala, S., & Hourihan, M.D.
2005.

pressing

case

of

transient blindness. British J of

Radiol, 78, 967-968.
19. Javad,
M.A.,
Hussain-Sial,
M.S.H.,

Lingawi,

S.,

Alfi,

A.,

Lubbad, E. 2005. Etiology of

posterior
encephalopathy

reversible
syndrome.

11 Neurological Department Faculty of Medicine ULM, Banjarmasin

Fakhrurrazy et al

Pakistan

Journal

of

Medical

Sciences Quarterly, 21(2), 149154.

20. Schneider, J.P., Krohmer S.,
Gunther A., Zimmer C. 2006.
Cerebral lesions in acute arterial
hypertension: the characteristic
MRI

in

encephalopathy.

Posterior

reversible

encephalopathy

prognostic utility of quantitative

diffusion-weighted MR images.
AJNR

Am

Neuroradiol;

23:10381048.
24. Garg, R.K. 2001.

Posterior

hypertensive

leukoencephalopathy syndrome.

Rofo;178:618

Postgrad Med J; 77:2428.

25. Casey, S.O., Sampaio R.C.,

626.
21. Brubaker, L.M., Smith J.K., Lee

Michel

E.,

Truwit

Y.Z., Lin W., Castillo M. 2005.

Posterior

Hemodynamics

encephalopathy

and

permeability

syndrome:

changes

in

utility

C.L.

2000.

reversible
of

syndrome:
fluid-attenuated

posterior

reversible

inversion recovery MR imaging

encephalopathy

syndrome

in the detection of cortical and

measured

by

dynamic

susceptibility

perfusion

weighted MR imaging.

Am J

Neuroradiol, 26, 825-830.

22. Gray, L., MacFall J. 1998.

subcortical

lesions.

Am

Neuroradiol; 21:11991206.
26. Stott,
V.L.,
Hurrell
M.A.,
Anderson TJ. 2005. Reversible
posterior

leukoencephalopathy

Overview of diffusion imaging.

syndrome:

Magn Reson Imaging Clin N Am;

reviewed. Intern Med J; 35:83

6:125138.
23. Covarrubias,
P.H.,

Campeau

89.
D.J.,
N.G.

Luetmer
2002.

misnomer