Neuroradiology (2004) 46: 1022–1026
DOI 10.1007/s00234-003-1129-3

J. K. Song
S. Fisher
T. D. Seifert
E. D. Cacayorin
A. V. Alexandrov
M. D. Malkoff
J. C. Grotta
M. S. Campbell

Received: 5 February 2003
Accepted: 2 October 2003
Published online: 27 November 2004
Ó Springer-Verlag 2004

J. K. Song (&)
Center for Endovascular Surgery,
Hyman-Newman Institute for Neurology
and Neurosurgery, 1000 Tenth Avenue,
New York, NY 10019, USA
E-mail: jsong@chpnet.org
Tel.: +1-212-8709660
Fax: +1-212-8709897

INTERVENTIONAL NEURORADIOLOGY

Postpartum cerebral angiopathy: atypical
features and treatment with intracranial
balloon angioplasty

Abstract Postpartum cerebral angiopathy (PCA) is an uncommon
cause of ischemic and hemorrhagic
stroke in young women. It is usually
clinically benign and not relapsing.
We describe a patient with nonhemorrhagic PCA who had an
atypical progressive neurological
deficit from bilateral hemisphere
watershed ischemia despite treatment with aggressive medical therapy and intracranial balloon
angioplasty.

Keywords Postpartum angiopathy Æ Angioplasty

E. D. Cacayorin
Interventional Neuroradiology,
Department of Radiology,
University of Texas Medical School,
6431 Fannin St, Suite 2100, Houston,
TX 77030, USA
S. Fisher Æ T. D. Seifert Æ A. V. Alexandrov
M. D. Malkoff Æ J. C. Grotta
M. S. Campbell
Division of Stroke Neurology,
Department of Neurology,
University of Texas Medical School,
6431 Fannin St, Houston, TX 77030, USA

Introduction
Pregnancy and the peripartum period are significant risk
factors for stroke in young women [1, 2]. The commoner
causes of stroke associated with pregnancy are venous
sinus thrombosis, subarachnoid hemorrhage (SAH)
from ruptured aneurysm or arteriovenous malformation, thromboembolism, vasculitis, migraine, coagulopathy, and pregnancy-induced hypertension. Postpartum
cerebral angiopathy (PCA), an uncommon condition,

can cause ischemic or hemorrhagic stroke [3]. It usually
responds to short courses of high-dose corticosteroids,
with rapid improvement and resolution of angiographic
findings within weeks of presentation [3, 4, 5]. Its pathogenesis and pathophysiology are unknown; it has been
suggested that it is a transient vasoconstriction in the
absence of SAH, or a continuum of true inflammatory
vasculitis [6, 7]. We describe a patient with strikingly
atypical features.

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decreased level of consciousness. Conventional cerebral angiography confirmed moderately severe narrowing of the supraclinoid segments of both internal

Fig. 1a, b Pretreatment imaging. a Initial CT shows bilateral low
density in the centrum semiovale, more marked on the right.
b Diffusion-weighted imaging nearer the vertex shows increased
signal consistent with acute or subacute ischemia of the right
centrum semiovale and distal cortical territory of the right anterior
cerebral (ACA)

Case report
A 42-year-old white woman, 8 days postpartum and
with no other significant past medical history, presented
with seizures and left-sided weakness. The pregnancy
and delivery were unremarkable, and she was not
hypertensive during her pregnancy or post-partum.
Imaging revealed an acute right watershed and pararolandic cortex infarct (Fig. 1a, b). Angiography revealed
diffuse arterial narrowing, with particular involvement
of the right anterior cerebral artery (ACA). The patient
was treated with dexamethasone, nimodipine, and
magnesium sulfate infusion. On arrival at our hospital
she was normotensive with a left hemiparesis (2/5 in arm
and leg). The cerebrospinal fluid was normal. Transcranial Doppler sonography (TCD) showed increased
velocities, predominately in the right middle cerebral
artery (MCA) distribution. The patient was placed on
triple H therapy: hypertension, hypervolemia, and
hemodilution.
MRI again showed the recent infarct; there was no
mismatch between perfusion and diffusion-weighted
images. MRA showed diffusely narrowed arteries in
both anterior circulations, with less severe narrowing
in the posterior circulation. The patient’s neurological
examination worsened with bilateral hemiparesis and a
c

Fig. 2a–c Internal carotid artery injections, frontal projections.
a Before treatment a right sided injection shows significant
narrowing of the distal supraclinoid, M1/M2 and A1 segments.
b The left side shows similar significant narrowing of same
segments. c After balloon angioplasty of the right supraclinoid
and M1 segments, their caliber is normal and circulation time is
faster

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carotid arteries, the right M1 and left A1 and A2
segments, and mild narrowing of the basilar artery
and proximal posterior cerebral arteries (Fig. 2).
We hen carried out balloon angioplasty of the right
M1 and the supraclinoid segments. Postangioplasty
injections showed successful dilation of both segments
(Fig. 2).
Comprehensive investigation was undertaken to
identify the source of the vasculopathy. Biopsy of the
right frontal lobe revealed microglial nodules and perivascular chronic inflammation but no thrombus, significant hyaline degeneration, mural deposits, or
evidence of active vasculitis. Despite improvement of
proximal perfusion after angioplasty, the patient was
unchanged neurologically. MRI the next day showed
extension of the right ACA and watershed infarct, plus
an acute left ACA and watershed infarct (Fig. 3a), although however, MRA confirmed that the right M1 and
supraclinoid segments remained patent.
The patient was continued on nimodipine, magnesium, steroids and triple H therapy. Serial TCD showed
gradually decreasing velocities, which then stabilized
(Fig. 3b). After 2 weeks, the patient began slowly to
improve, following simple commands and moving her
arms spontaneously; she patient was transferred to a
rehabilitation facility where she continued to improve,
moving her toes and fingers and following complex
commands.

Fig. 3a,b Follow-up imaging. a Diffusion-weighted imaging 6 days
after apparently successful angioplasty there is progression of
bilateral, predominantly watershed territory ischemia, with confluent restricted diffusion in both centra semiovalia. Right frontal low
signal is due to hemorrhage after brain biopsy. b Graph showing
mean velocities on transcranial Doppler sonography in the right
and left M1 segments with respect to time of angioplasty

Discussion
PCA is a relatively rare cause of ischemic stroke in
young women. The few available reports of nonhemorrhagic focal neurological deficit in postpartum women
have described associations with labile hypertension,
pre-eclampsia, and vasospastic drugs such as ergonovine, bromocriptine, and sympathomimetics [2, 8, 9, 10,
11, 12]. In the remaining cases, the diagnosis of ischemic
PCA was presumed, as no etiology was found despite
extensive investigation for risk factors, with cerebral
angiography showing multiple intracranial vessels stenoses and ectasia, suggesting diffuse spasm or vasculitis
[4, 6, 7, 13]. The clinical course of PCA is typically benign, with resolution, sometimes rapid, of neurological
deficits [3, 4, 7].
We found one other report of ischemic PCA with an
aggressive clinical course. Geraghty et al. [6] reported a
27-year-old woman who presented on postpartum
day 13 with intermittent, then persistent left hemiparesis, with MRI (without diffusion-weighted imaging) at
16 days showing no evident abnormality. Angiography
revealed widespread, mild, irregular stenoses proximally
and distally. Despite treatment with corticosteroids, the
patient deteriorated, CT revealing bilateral cortical infarcts in the right ACA and posterior left MCA territories. She subsequently became comatose, CT then
showing diffuse edema with extensive bilateral MCA
and left ACA infarcts that led to death. Our patient
differed in that the proximal vessels were markedly more
involved, similar to the picture seen in vasospasm from
aneurysmal SAH. Stenoses of the proximal supraclinoid
carotid, M1, and A1 segments probably led to perfusion
compromise and watershed ischemia rather than extensive cortical MCA and ACA infarcts. TCD indicated
worsening stenoses in the proximal MCA territories.
Diffusion-weighted MRI clearly demonstrated the acute/
subacute ischemic nature of the confluent bilateral

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centrum semiovale white matter and distal right ACA
cortical low density seen on CT. In one report of a 39year-old woman with hemorrhagic PCA, bilateral centrum semiovale ischemic changes were also suggested [3];
however, the lesions were focal, small and not confluent
and the patient recovered almost completely within a
week of treatment with corticosteroids.
Treatment for PCA has typically consisted of corticosteroids, but calcium channel blockers, aspirin,
cyclophosphamide, and intravenous nitrogen mustard
have been used [3, 6, 7]. As our patient unexpectedly
worsened despite corticosteroids, triple H therapy was
instituted, using the same protocol as for symptomatic
vasospasm from SAH. Despite maximal medical therapy, she continued to deteriorate. Velocities of both
MCA territories continued to increase, indicating severe
narrowing of the right proximal MCA (mean velocity>200 cm/s). Despite the poor selection criteria for
intracranial balloon angioplasty [14] (low density on CT,
>12 h of worsening symptoms, uncertain correlation of
neurological deterioration and implicated vessel segment), intracranial balloon angioplasty was carried out,
using the technique employed for SAH-related vasospasm. To achieve mechanical vessel dilation, we used a
higher-pressure low profile balloon (2.5 mm in diameter,
15 mm long).
Experimental data suggest that acute hypertension
can produce areas of vasospasm and dilation [11], and
transient hypertension has been a feature of some reported cases of PCA [4, 9]. This may suggest that vessel
narrowing might be protective and dilation using
angioplasty might actually interfere with this protective
mechanism. Although it may contribute to the generally

relatively benign course of PCA, in our patient this
‘‘protective’’ mechanism was causing worse, debilitating
watershed infarcts, and angioplasty was therefore pursued with the goal of salvaging any ischemic penumbra.
It has been hypothesized that PCA is a hormonally
mediated effect on the intima precipitated by acute elevations in blood pressure [6, 15, 16], and this is supported by the autopsy findings of slight intimal
proliferation [6].
Calabrese et al. [7] suggested that PCA may represent
a continuum of vascular pathology with initial vasospasm leading to vasculitis. As it is not known whether
PCA is an inflammatory vasculitis, balloon angioplasty
in this setting was of questionable utility. McKenzie
et al. [17] described in four patients with presumed
vasculitis in whom they had poor results, as all five
segments on which they carried out balloon angioplasty
progressed to occlusion within 48 h, after initial
improvement. In our patient, as the dilation of the right
M1 MCA and supraclinoid internal carotid artery after
balloon angioplasty lasted for more than 7 days, the
response of the vessels in PCA to angioplasty appears
different from that in vasculitis. Despite the technical
success of angioplasty, the ischemic damage extended,
probably because the tissue was no longer viable at the
time of angioplasty. As in the setting of acute thromboembolic stroke and symptomatic vasospasm, the
timing of intervention is crucial in determining whether
reperfusion leads to reversal of ischemia and salvage of
penumbra or to no change in outcome. Given the vessel
response to balloon angioplasty, earlier, more aggressive
balloon angioplasty might have improved the clinical
outcome of our patient.

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