Timothy

G. Sanders, S. Vines,

Frederick

Brain with

MD MD

David A. Clayman, Louis Russo, MD

in Eclainpsia: MR Clinical Correlation’

Cranial imaging secutive

magnetic resonance (MR) was performed on eight conpatients with generalized tonic-clonic seizures caused by eclampsia. Each patient underwent serial neurologic examinations until all symptoms resolved. Six of those eight patients underwent follow-up MR imaging. These patients were compared with those in previous case reports of MR imaging abnormalities of the brain in eclampsia. MR imaging typically demonstrates bilateral hyperintense lesions on T2-weighted images and iso- to hypointense lesions on Ti-weighted images. MR imaging abnormalities are most commonly located in the distribution of the posterior cerebral circulation and are associated with visual disturbances. Basal ganglia and deep white matter lesions are less common and are associated with mental status changes. Most lesions seen at MR imaging in patients with eclampsia are reversible. Index terms: Brain, abnormalities, 10.919 #{149} Brain, MR studies, 10.1214 #{149}Pregnancy, cornplications, 10.919, 85.131 1991;

180:475-478

From the Departments of Radiology (T.G.S., D.A.C., F.S.V.), ObstetricWGynecology (L.S.R.), and Neurology (L.R.), University of Florida Health Science Center/Jacksonville, 655W Eighth St,Jacksonville, FL 32209. From the 1990 RSNA scientific assembly. Received December 17, 1990; revision requested February 12,1991; revision received March 8; accepted April 1. Address reprint requests to T.G.S. 0

RSNA,

1991

Sanchez-Ramos,

MD

Imaging

a hypertensive disorder of pregnancy occurring after the 20th week of gestation, is characterized by hypertension, peripheral edema, proteinuria, and seizures (1) and is a relatively common medical problem. Because magnetic resonance (MR) imaging will probably soon become the imaging modality of choice to evaluate the brain in patients with edampsia, it is important to recognize the typical lesions seen at MR imaging and the natural course of the lesions.

Neurologic

complications

in

patients with eclampsia are varied and include headache, visual disturbances, focal neurologic deficits, altered mental status, and coma (2). Treatment goals of edampsia include the (a) promotion of adequate renal function, (b) control of seizures, (c) control of blood pressure, and (d) termination

of pregnancy

as the

decisive

step of therapy. The maternal mortality rate for properly treated eclampsia is less than 5% (1). Several recent case reports have described lesions of the brain in isolated cases of edampsia with MR imaging (3-11). Eight patients with edampsia UnMR

imaging

evaluation

of

the brain and are compared with those described in previous case reports. The purpose of our study was to describe the typical MR imaging patterns and associated dinical findings of eclampsia, as well as the pathophysiologic features of the central nervous system (CNS) lesions. PATIENTS

I

Luis

#{149}

E

derwent Radiology

MD

#{149} #{149}

AND

METHODS

The study was planned prospectively, with all MR images reviewed prospectively. Eight consecutive obstetric patients with eclampsia were referred to the department of radiology for evaluation of the brain with MR imaging during an 18month period (Table). Each patient fulfilled the diagnostic criteria for edampsia, with documented generalized seizures, hypertension (blood pressure greater than 140/90 mm Hg), proteinuria, and periph-

eral edema. None had a history of seizures. In each case, MR imaging was initially performed within 4 days of the onset of seizures. Patient 6 was in her 37th week of pregnancy when she underwent MR imaging. The remaining seven patients were post partum at the time of the initial MR imaging. MR images were obtained with a 1.0-T magnet (Vista-MR 2055 HP; Picker, Cleveland) with TI-weighted (spin-echo [SE] 733,20 [repetition time mseclecho time msec]) and T2-weighted (SE 3,000/20-80) multiecho sequences, with 6-mm-thick axial sections and a 2-mm gap. No patient received

gadopentetate

dimeglumine.

Computed tomography (CT), performed only on patient 1, revealed no abnormalities.

The medical were reviewed any neurologic

records of each patient to determine if there were defldts at the time of the original MR imaging and to determine whether any permanent neurologic deficit remained. Although documentation of the neurologic status was available for each patient,

a formal

neurology

consultation

was not performed in every case. Six of the eight patients underwent follow-up MR imaging. The time interval for these follow-up studies ranged from 2 to 5 months following the initial MR examination. Follow-up MR imaging was not performed on the patient whose original study yielded normal results (patient 6), and one patient (patient 3) refused follow-up examination. RESULTS Clinical

Findings

The initial neurologic examinations revealed visual disturbances in five the eight patients (Table). Four of these

patients

experienced

only

blurred vision deficit (patients tial examination,

with no visual field 2-4 and 8). At the patient 1 had

blurred

vision,

which

cortical

blindness.

Abbreviations: SE = spin echo.

CNS

progressed

In all patients,

=

of

central

nervous

mi-

to

the

system,

475

MR Imaging-Clinical

Correlates

in Eight Patients

Patient

Eclampsia

with

Blood

No/Age

(y)

Parity

Location

Pressure

Neurologic

(mm Hg)

Symptoms

1/33

Gravida

2, para 2

140/100

Corticalblindness

2117

Gravida

1, para

160/130

Blurred

1

Lesions

vision,

of

Residual

at Initial

Follow-up

Neurologic

MR Imaging

MR Imaging

and

Clinical

MR Imaging

Deficit

Findings

Correlation

Occipital, parietal, temporal Occipital, parietal

None

Total resolution

Yes

None

Total resolution

Yes

Occipital, frontal

None

No follow-up

Yes

None

Total resolution

No

None

Total

No

None

No follow-up

Yes

None

Total resolution

Yes

None

Total resolution

Yes

no focal deficit 3,20

Gravida

1, para 1

168/110

Blurred vision, headache, no focal

parietal,

4/17

Gravida

1, para 1

140/100

Dystaxia,

156/103

disconjugate gaze, blurred vision None

Left

Headache,

left temporal, periventricular white matter None

deficit

Gravida

5t22

1, para

I

W23

Gravida

1, para

1

150/96

7/28

Gravida

3, para

3

190/98

8/17

Gravida

2, para 2

220/180

visual acuity returned to normal 1evels in less than 10 days after the original examination. Only patient 4 developed focal neurologic deficits other than visual disturbances, including dysarthria, dystaxia,

and

developed zure. These within

a disconjugate

gaze

after the generalized focal deficits resolved

that

sei-

9 days.

The three remaining patients (patients 5-7) developed no neurologic symptoms; normal results of a neurologic examination were recorded in each

case.

plained

6 and

of postictal

resolved

MR

Patients with

Imaging

7 com-

headaches,

symptomatic

which treatment.

Findings

All patients underwent initial MR imaging within 4 days of seizure activity. Follow-up examinations were performed in six of the eight patients between 2 and 5 months after the mitial MR examination. In each instance, the follow-up MR image revealed total resolution of the original abnor-

malities. The

initial

MR

image

of patient

6

was obtained approximately 24 hours after the onset of eclampsia and was normal; thus, no follow-up study was required. In patient 3, abnormalities were found on the original MR image, but she refused to return for a follow-up study. Her follow-up clinical

Parietal

dysarthria,

no focal deficit Headache, no focal deficit Blurred vision, no focal deficit

dual-echo In most better

SE T2-weighted sequence. cases, the abnormalities were with

However, were seen

tense with cortical weighted images. MR

476

Radiology

#{149}

of a

on Ti-

ings correlated abnormalities. velop

a focal

with the MR imaging Patient 6 did not de-

and

of MR

in the

team

did not appear to correlate. Pa4 developed dysarthria, dystaxia,

parietal would

gaze, bilateral

which

do

cortical

lobe lesions. The symptoms correlate most closely with

two

In five

found

supratentorial

no

focal

neuro-

patients.

patients

abnormalities nor parietal

(patients

were and/or

i-4

a

and

8),

seen in the posteoccipital regions.

These lesions were predominantly located in the subcortical white matter, with occasional involvement of the cortex. In each instance, the lesions

were

bilateral

The

lesions

were

cm

long

sions lobes, ment

cortical cortical

In two patients, the clinical findings the lesions visualized on MR im-

with

and

and

periventricular white matter. Despite the presence of extensive lesions in the region of the left basal ganglia, the

and

and

symmetric.

typically

produced

patient

less no

than

mass

8 exhibited

3

effect.

le-

in both the frontal and temporal patients 1 and 5 had involveof the temporal lobes, and pa-

tient 3 developed frontal The frontal and temporal were generally confined

and

had a normal MR image. In each the above cases, the clinical and imaging findings correlated.

putamen,

capsules

logic deficit. Hence, correlation between the clinical findings and MR imaging abnormalities was lacking in

Correlation

deficit

external

abnormalities

obstetric

neurologic

pallidum,

and

In addition,

a disconjugate

echoes

matter

globus

internal

matter. Small lesions in these areas would be unlikely to cause focal deficits; therefore, the lack of clinical find-

correlate

both

gray

date,

these

not

on

le-

at first

resolution

lesion of the posterior fossa. However, the MR image demonstrated no abnormalities in this region. The MR image of patient 5 demonstrated extensive abnormalities in the left cau-

parietal identified on who developed visual disturbances (patients i-4 and 8). In this group, the locations of the lesions correlated with the clinical findings. Patient 7 did not demonstrate either visual disturbances or focal neurologic deficits; MR imaging abnormalities were confined to the supratentorial periventncular white

and

hyperintense

well

Lesions in the posterior and occipital areas were MR images in all patients

In seven patients, abnormalities were found on the initial MR images. In all instances, the lesions were

no focal acuity.

the second cases, the

Imaging-Clinical

ages tient

revealed visual

in two equally

and second echoes. In five of the seven patients, the lesions were hypointense on Ti-weighted images. In the remaining two patients, the lesions were located in and were isoin-

deficits

examination and a normal

ganglia,

Periventricular white matter Frontal, occipital, temporal

visualized

echo. sions

basal

white matter, involvement.

lobe lesions. lobe lesions to the sub-

with These

occasional lesions

were less symmetric than those in the parietal and occipital lobes. Patients 5 and 7 had lesions in the supratentorial periventricular deep white matter. In addition, patient 5 developed lesions in the left basal ganglia. These lesions were globular and

measured

less

than

1.5 cm

August

in di-

1991

several lopathy, :

w_

Y

mechanisms, perivascular

rhage,

perivascular

edema,

hypoxic

cerebral graphic eclampsia spread

.r

t,

5

pathologic transient cerebral

k1M

Figure 20-80) malities

Figure 1. T2-weighted MR image (SE 3,000/ 20-80) in patient 1 demonstrates hyperintense lesions in occipital lobes bilaterally. Clinically, patient developed complete cortical blindness.

3. 12-weighted MR image (SE 3,000/ in patient 5 reveals extensive abnorin left basal ganglia. This patient did

not develop

intra-

herein. of patients

The clinical with ec-

lampsia and hypertensive encephalopathy are very similar, and findings of MR imaging in both groups support the concept that the clinical and

-

‘

and

these vascular changes unplay a role in the CNS le-

sions described presentations

‘1

microinfarcts,

ischemia,

hemorrhage (12). Angloevaluation of patients with has demonstrated wideintracranial vasoconstriction

(13), and doubtedly

1p

including vascumicrohemor-

neurologic

findings disruption autoregulation,

in extravasation across

an

are a result of of the normal which results

of fluid

altered

and

blood-brain

proteins barrier

(3-5,14-16).

In our series of patients, the lesions visualized at MR imaging were all hyperintense on both echoes of a

symptoms.

dual-echo and were

SE T2-weighted sequence either iso- or hypointense

on Ti-weighted images. Follow-up examination, when performed, revealed complete resolution of all lesions. No hemorrhage or permanent CNS

signal lesions, -4’ 4-

;

V Figure 20-80)

4. 12-weighted MR image (SE 3,000/ in patient 7 demonstrates bilateral hyperintense lesions in periventricular white

matter 2. T2-weighted MR image in patient 2, who developed demonstrates hyperintense lobe lesions.

(SE 3,000/ blurred bilateral

velop

bilaterally.

This

neurologic

patient

did not de-

symptoms.

CT may be indicated mitially to exclude intracranial hemorrhage. Patients with a normal head CT scan and a focal neurologic deficit should then undergo MR imaging. The typical patient who demonstrates only visual disturbances should probsciousness,

Abnormalities

ameter.

in these

areas

were bilateral but were much symmetric than those lesions parietal and occipital lobes.

less in the

ably

DISCUSSION Patients variety

with from

casionally,

includes bances

with logic such

Volume

eclampsia

of neurologic

ranging

a variety In the

develop

a

complications,

headache

a focal (2).

of the

to coma.

neurologic

of visual eclamptic

Oc-

deficit

disturpatient

hypertension and a focal neurodeficit or signs of mass effect, as a decrease in the level of con180

Number

#{149}

2

was

demonstrated.

The

intensity characteristics of these and the fact that all abnormal-

ities

resolved,

that

these

support

lesions

the

concept

represent

leakage

of

fluid across a transiently abnormal blood-brain bamer. However, these same findings could be secondary to increased intracellular fluid from a

\qJ

Figure 20-80) vision, parietal

lesion

undergo brain.

MR

imaging

In the

evaluation

patient

with

complicated eclampsia and neurologic deficit, imaging be required. The exact pathophysiologic changes in patients

leading with

certain. A recent logic correlation tual CNS lesions

to CNS eclampsia

un-

no focal may not

abnormalities remain

transient cellular ischemia, which may better explain the lesions seen in the basal ganglia. The MR images in our series showed no evidence of microhemorrhage or microinfarct, as demonstrated pathologically in previous case reports (i2). This may be attributed to the fact that these lesions are microscopic and below the limit of resolution of the MR imager. Another explanation may be that these patients experienced

study with pathosuggests that the acmay be attributed to

severe

clinical

permanent case report

brain ischemia (6-8). described a hemorrhagic

lesion

hemosiderin

seen

examination

(5).

low-up un-

a less

course and did not develop the microhemorrhages seen in patients studied pathologically. A few case reports have described persistent hyperintense lesions on T2-weighted images that may actually represent areas of

with MR

One

at fol-

A computer search of the literature with the Grateful Med program of the National Library of Medicine revealed nine case reports within the past iO years describing MR imaging abnorRadiology

#{149} 477

malities of the brain in eclampsia (311). These nine case reports included 14 patients with eclampsia and one patient with preedampsia (hypertension, edema, and proteinuria in pregnancy

not

accompanied

by seizures

[1]). The combination of our series and the previous case reports reveals two areas of the brain that frequently demonstrate MR abnormalities. The most common location of involvement is the region of the posterior cerebral circulation (Figs 1, 2). These lesions are present in the cortex and subcortical white matter and involve the occipital and posterior parietal lobes. They are bilateral and symmetric and follow the gyri in a serpentine manner.

No

der

infarct

zone

identified,

other

evidence

pattern

and

only

of a bor-

has

a single

been case

re-

port of a posterior fossa lesion is present (6). Five of eight patients in our series and all patients from the case reports had involvement of these areas (3-11). A second area that commonly demonstrates an abnormality on MR images is the deep white matter and basal

ganglia

(Figs

3, 4). As in the

first

group, the lesions are bilateral; unlike the first group, the lesions of the deep white matter and basal ganglia lack symmetry. The lesions are globular or linear,

as opposed

to the

serpentine

lesions in the cortical and subcortical locations. Two patients in our series and five patients in prior case reports demonstrated abnormalities in these areas (5-7,9,11). The reason for predilection of lesions to these two areas is uncertain. It has been shown that CNS lesions in hypertensive

disorders

are

secondary

to extravasation of fluid across an abnormal blood-brain barrier (15,17-19). At present, no significant data suggest regional differences in blood-brain barrier permeabifity. However, from the findings described herein, a hypothesis

of increased

permeabifity

secondary to loss of autoregulation in the posterior cerebral circulation, basal ganglia, and deep white matter may be considered. The region of the posterior cerebral circulation correlates closely with the clinical findings of visual disturbance.

References

In our series, every patient who developed abnormalities in either the occipital or posterior parietal lobes also complained of visual disturbances. In the literature, seven of 15 patients with MR imaging abnormalities in these regions demonstrated signs and symptoms of visual disturbances.

No

patient

developed

1.

Book, 1979;

2.

status.

These

3.

4.

increased

intracellular

fluid

secondary

to a transient cellular ischemia. Two typical patterns are seen on MR images of patients with eclampsia. The subcortical lesions in the region of the posterior cerebral circulation are most common

and

are

frequently

6.

9.

with

mental

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BA, Sandson

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tomographic

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Dinsdale HB. Hypertensive encephalopathy. Neurol Clin 1983; 1:3-16. Rail DC, Perkin GD. Computerized tomographic appearance of hypertensive encephalopathy. Arch Neurol 1980; 37:310311. Auer LM. The pathogenesis of hypertensive encephalopathy: experimental data and their clinical relevance with special

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eclampsia:

correlate

more

ME.

576. 8.

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changes.

Healy

of revers-

eclampsia.

7.

ated with visual disturbances. Lesions in the deep white matter or basal ganglia are less commonly identified and status

report:

211-250.

70:474-477.

5.

findings

range from confusion to coma in the reported cases (5,6,9,11). Although none of the patients in this series demonstrated a change in mental stahis, four of five patients from the literattire with lesions in these regions developed alterations in mental status. MR imaging abnormalities are demonstrated less frequently in the frontal and temporal lobes, with a single report of cerebellar involvement (35,8,9). No clinical findings can be consistently attributed to lesions located in these areas. MR imaging has also demonstrated lesions in several patients who did not develop a focal neurologic deficit (3,4,10). Patient 5 in our series demonstrated extensive abnormalities in the left basal ganglia, and yet no clinical abnormalities were noted. These cases demonstrate the sensitivity of MR imaging in the detection of abnormalities in patients with eclampsia, even those without neurologic deficits. Our series of patients, combined with a review of the literature, supports the concept that most CNS lesions in eclampsia represent either reversible edema from transient alterations in the blood-brain barrier or

of pregnancy.

Neurology Saunders, 1978; BW, HesselinkJR, MR demonstration

Schwaighofer Case

visual

clinical

335-348.

DonaldsonJO. Philadelphia:

disturbances without exhibiting a lesion in this region. MR imaging abnormalities in the deep white matter or basal ganglia correlate more dosely with changes in mental

Wilson JR, Carrington ER. Obstetrics and gynecology. 6th ed. St Louis: Mosby-Year

to neurosurgical (Wien) 1978;

Skinhoj E, Strandgaard S. hypertensive encephalopathy.

Pathogenesis

of

Lancet 1973;

1:461-462.

We thank

Acknowledgment

her always

478

#{149} Radiology

excellent

manuscript

Carole

Welsh

for

preparation.

August

1991