Journal of Neurology, Neurosurgery, and Psychiatry 1989;52:899-902

Blindness in eclampsia: CT and MR imaging
RODERICK DUNCAN, DONALD HADLEY, IAN BONE, E M SYMONDS,
B S WORTHINGTON, P C RUBIN
From the Institute of Neurological Sciences, Southern General Hospital, Glasgow and University Hospital,
Nottingham NG7 2UH
SUMMARY Three cases of cortical blindness complicating eclampsia are described, with magnetic
resonance imaging (MRI) and X-ray computed tomography (CT). The correspondence of MRI

lesions (hyperintense on T2 weighted, and hypointense on T, weighted sections) and low attenuation
lesions on CT scan indicated ischaemia rather than haemorrhage as the pathological mechanism.
Reversible focal neurological lesions are a rare feature
of eclampsia, most reports being of patients with
cortical blindness. Where X-ray computed tomography (CT) has been carried out, this has either shown
low attenuation lesions in the occipital cortex,'1"7
multiple low attenuation lesions,67 or has been normal.'2-15 We present three cases ofblindness complicating eclampsia, and discuss CT and magnetic resonance
imaging (MRI) findings.
Methods

Unenhanced CT was carried out using a Philips 310 Tomoscan, producing 6 mm axial cuts parallel to the orbito-meatal
line. Corresponding T2 weighted (SE 2000/120) and T,
weighted (IR 1600/400/40) 8 mm thick axial MRI sections
were obtained using a Picker 0-15 Tesla resistive imager.
Case 1
A 38 year old para 1 + 0 in the 38th week of pregnancy was
admitted to hospital with a history of acute visual loss and
frontal headache. She had been hypertensive during her first
pregnancy and had no past history of migraine. The visual
loss had woken her in the morning, and had progressed over
two hours until she was blind. On admission to hospital, she
was hypertensive with a blood pressure of 165/120 mm Hg,
and proteinuric. She had a tonic/clonic seizure, eclampsia
was diagnosed and a caesarean section was performed.
On transfer to the Regional Neurological Unit, she was
drowsy, but oriented. She could perceive only strong light,
but pupillary responses were normal. There was a conjugate
palsy of upward and left lateral gaze. Tendon reflexes were
exaggerated with clonus in the left leg. Plantars were
downgoing. Vibration sense was absent below the waist, but
sensory testing was otherwise normal. There were no rashes
Address for reprint requests: Dr Duncan, Institute of Neurological
Sciences, Southern General Hospital, Glasgow G51 4TF, UK.
Received 17 November 1988 and in revised form 3 February 1989.
Accepted 6 February 1989

Fig 1 Case 1: axial T2 weighted MR image showing high
signal lesions at both occipital poles (arrows).
or other clinical evidence of systemic vasculitis. Blood
pressure was 138/95 mm Hg.
ESR was raised to 86 mm in the first hour, she had a
platelet count of 137 x 109/mm3, and a urea of 7 4 mmol/l.
Fibrin degradation products, and a clotting screen were
nonnal. Autoantibody studies were negative. Cranial CT
performed on admission showed no abnormality.
Her vision and abnormal neurological signs recovered to
normal over 24 hours, despite continuing poor control of her
blood pressure. MRI was performed on day 3 and showed

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Duncan, Hadley, Bone, Symonds, Worthington, Rubin
..i.
......
ii

Fig 2 Case 2: axial unenhanced CT imnage showing low
density in the right occipital lobe. A higher section showed a
similar lesion on the left (arrow).
focal lesions in both occipital poles. These were non-space
occupying and gave a hyperintense signal on the T2 weighted
images, and a hypointense signal on the T, weighted images
(fig 1). Follow up MRI performed 2 months later showed
complete resolution of the occipital lesions.
Case 2
A 20 year old para 0 + 0 had a caesarean section at 34 weeks
for severe pre-eclampsia, diagnosed on the basis of hypertension, proteinuria and headache. She had no past history of
hypertension or migraine. Post partum her blood pressure
remained high despite treatment with atenolol, intermittently
reaching levels as high as 200/100 mmHg. The fourth evening
post partum she became confused and complained of severe
frontal headache. The next morning she was alert and
oriented, but her headache persisted. Over three hours he
vision deteriorated until she was blind. She was transferred to
the Regional Neurological Unit, where she suffered 2 tonic/
clonic seizures. On examination, blood pressure was 165/110
mmHg. The fundi were normal, as were eye movements and
pupillary reflexes. Vision had improved to perception of
bright light throughout the visual fields. Neurological
examination was otherwise normal.
Routine haematological and biochemical tests were normal. Cranial CT on admission showed bilateral occipital low
attenuation lesions (fig 2). MRI carried out on the day of
admission showed several focal non-space occupying lesions,
hyperintense and hypointense on the T2 weighted and T,
weighted images respectively. These lay in both occipital
lobes in the right posterior temporal cortex (figs 3 and 4), and

Fig 3 Case 2: axial T, weighted MR image showing low
signal lesion in the left temporal lobe (arrow).
in the white matter of the left temporal and occipital lobes,

extending into the lateral cortex.

Vision returned to normal within 36 hours, despite her
blood pressure remaining poorly controlled. Follow up MRI
carried out 6 weeks later showed complete resolution of the
occipital lesions, and near complete resolution of the temporal lesion.
Case 3
A 26 year old para 1 + 0 was admitted at 18 weeks gestation.
Her previous pregnancy had been unremarkable, but
ultrasound examination in this pregnancy carried out at 14
weeks had suggested foetal abnormality. She had been well
until a few hours prior to admission when she had two tonic/
clonic convulsions. She regained consciousness but then
developed complete blindness over two hours. There was no
history of migraine. On examination, visual acuity was
limited to the perception of bright light. Fundal examination
and pupillary responses were normal, as was the remainder of
the neurological examination. Blood pressure was 150/90
mmHg, and she had proteinuria. Eclampsia was diagnosed,
and the pregnancy terminated the same day.
Routine haematological and biochemical tests were normal, as was cranial CT performed on the day of admission.
MRI performed on day 3, at which time visual acuity had
recovered to counting fingers, showed a focal non-space
occupying lesion in the right occipital pole, hyperintense and
hypointense on the T2 weighted and T, weighted images
respectively (fig 5). Necropsy on the foetus revealed
holoprosencaphaly and a molar placenta.

.j,_~ ~.

Blindness in eclampsia: CT and MR imaging

Fig 4 Case 2: axial T2 weighted MR image showing high
signal lesion in the white matter ofthe left temporal lobe
corresponding to the lesion seen in fig 3 and in the left
occipital lobe (arrows).

Fig 5 Case 3: axial T2 weighted MR image showing a high
signal lesion at the right occipital pole (arrow).
Her vision returned to normal over 3 days, despite poor
blood pressure control. Follow up MRI done 3 months later
was normal.

901

Discussion
In all three cases the diagnosis of eclampsia seems
certain, with hypertension, proteinuria and seizures
occurring in association with pregnancy. Although
Case 3 occurred at 18 weeks, this was in association
with molar degeneration, an established risk factor for
early eclampsia.'6 Despite the statistical association
between the two conditions," none of our patients had
a history of migraine.
Blindness due to eclampsia may be due to lesions at
any site along the visual pathway, but the majority of
case reports are of cortical blindness. Although there
were minor retinal changes in Case 1, intact pupillary
reflexes and the radiological finding of occipital cortical lesions in our cases confirm that they too were of
cortical origin. The majority of patients with cortical
blindness due to eclampsia recover vision, over a
period varying from 2 hours to 21 days '-15 1122 although there is one reported case ofpersistent deficit.5 In
Case I blindness was the presenting feature of eclampsia, while in Case 2 it occurred 5 days post partum.
Approximately 50% of the cases in the literature have
occurred post partum,48912'3202' by up to 7 days.'3
Blindness was the presenting feature of eclampsia in
six cases. 27121113 15
Clinically, there also were lesions at other sites in
Case 1. The finding of gaze palsies indicated a low
midbrain/high pontine lesion. The sensory level to
vibration sense suggested the possibility of a spinal
cord lesion, as did the findings of increased reflexes
and clonus. In the other two cases there was no clinical
evidence of focal lesions other than those in the
occipital cortex. In cases in the literature, increased
tendon reflexes are common,346712152122 and are not
always associated with seizures. More definite
evidence of pyramidal dysfunction such as ankle
clonus, upgoing plantars and hemiparesis is also
found,34'42' as are gaze palsies,37 nystagmus7 and
fluent dysphasia.'3 In one case cortical lesions on CT
coexisted with bilateral retinal detachments.9
Most recent reports feature the results of CT, and
this either was normal,7121315 showed focal low attenuation occipital lesions,'-5 9" or more widespread low
attenuation lesions.67 The lesions were non-enhancing, and were ascribed to localised oedema or to
infarction. Repeat CT has shown partial resolution of
lesions in 3-5 days2 37 and complete resolution in 9-14
days.'69'0 A recent report24 describes the results of
MRI in a single case of eclampsia. Although clinically
the patient had no focal neurological features, lesions
with similar signal characteristics to those seen in our
cases were shown in the right occipital lobe and left
parietal lobe. They had resolved by the time a further
scan was carried out 3 weeks post partum, and were
ascribed to localised oedema. They were not detected
by CT. CT and MRI findings in hypertensive encephalopathy are similar.24
Our MRI findings are consistent with those in

902
transient ischaemic lesions,25 and reflect focal increases
in brain water content,26 which may persist for several
days after the resolution of neurological signs.27 This
results in increases in T, and T2 relaxation times, giving
hypointensity on T, weighted images and hyperintensity on T2 weighted images. In contrast, acute focal
haemorrhage gives a hypointense signal on T2 weighted images or, at the subacute stage, a hyperintense
signal on T, weighted images.
In the large necropsy series of Sheehan and Lynch28
and Govan1' gross haemorrhage was the most
frequent cause of death, but the most common finding
was of cortical groups of small (0 3-1 mm) haemorrhages associated with infarcts of similar size. It seems
likely that our findings represent such lesions, and that
they are primarily ischaemic rather than haemorrhagic. Small haemorrhages are seen in the placental
vascular bed in eclampsia, and ultrastructural studies
suggest that they are secondary to ischaemic vascular
damage.30
Angiographic studies in eclampsia show generalised
large vessel spasm,31 and tend to support the view that
ischaemia is the cause of focal neurological dysfunction. However, angiographically demonstrated spasm
does not always relate well to cerebral blood flow,32
and spasm may occur without ischaemia and vice
versa.
The finding of ischaemic lesions in eclampsia suggests that aggressive treatment of hypertension is
likely to exacerbate neurological damage. It would
appear that the most appropriate treatment in such
cases would be a drug with cerebral vasodilator
activity such as nifedipine. Alternatively, a more
specific cerebral vasodilator agent such as nimodipine
might be used in conjunction with other antihypertensive agents.
We thank the obstetricians and neurologists who
looked after our three patients for allowing us to
report them. The MRI Unit was funded by grants
from the Medical Research Council and other bodies.
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