Post-partum cerebral angiopathy: Repetitive
TCD, MRI, MRA, and EEG examinations
Peter Zunker*, Kirstin Golombeck{, Joachim Brossmann{,
Dimitrios Georgiadis§ and Günther Deuschl*
*Department of Neurology, { Department of Gynaecology, {Department of Radiology, Kiel University Hospital, Kiel
§
Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany

We report of a woman with post-partum cerebral angiopathy (PCA), in whom we repetitively performed
transcranial Doppler sonography (TCD), MR imaging (MRI), and MR angiography (MRA) to evaluate the
underlying pathophysiology. A 31-year-old woman, Gemini pregnant, complained of severe throbbing
frontal headache four days after an uneventful delivery by Cesarean section. Blurred vision occurred eight
days after delivery, followed by three generalized tonic–clonic seizures. Neurological examination
revealed a somnolent woman without focal neurological deŽcits. At the day of the seizures increased ow
velocities and disturbed ow were observed in the right posterior and anterior cerebral artery on
transcranial Doppler (TCD). MRI showed infra- and supratentorial patchy hyperintensities in T2-weighted
images and in the FLAIR sequence. Diffusion-weighted imaging revealed corresponding multi-focal
hyperintense areas indicating increased diffusion and MRA showed a diffuse multisegmental narrowing of
all pial arteries. MRI at day 10 was completely normal, but MRA still revealed vascular narrowing in the
right posterior cerebral artery. General slight ow accelerations in all basal arteries occurred after 10 days
and lasted for three weeks. PCA is apparently associated with a vascular narrowing causing cerebral
ischemia with increased diffusion. Later reactive cerebral hyperperfusion is observed. Vascular narrowing
and cerebral hyperperfusion still persist after MRI has normalized. [Neurol Res 2002; 24: 570–572]
Keywords: Eclampsia; cerebral perfusion; post-partum cerebral angiopathy; therapy

INTRODUCTION
Post-partum cerebral angiopathy (PCA) is characterized
by the occurrence of severe throbbing headache, altered
consciousness, vomiting, seizures and focal neurologic
signs few hours to one month after a normal pregnancy1 .
The typical vascular Žndings consist of a multi-segmental narrowing of the cerebral arteries1 ,2 . PCA is
associated with intracerebral hemorrhage2, 3, ischemic
stroke4,5 or focal edema1,6,7 . We report on a woman
with PCA, in whom transcranial Doppler (TCD), MRI,
inclusive diffusion-weight-imaging, MR-angiography,
and EEG were repetitively performed in order to evaluate
the underlying pathophysiology.
CASE REPORT
A 31-year-old woman, Gemini pregnant, was subjected
to Cesarean section at the 36th week of gestation due to
a post-renal drainage impairment with slightly elevated
plasma concentrations of creatinine and urea. The
patient had no vascular risk factors and there was no
history of migraine. Pregnancy was uneventful until
post-renal drainage impairment was diagnosed; in
particular, no arterial hypertension or proteinurea were
observed. Serum concentrations of creatinine and urea
normalized within three days. The patient received
Correspondence and reprint requests to: Peter Zunker, PhD, MD, ItaWegman-Hospital, 4144 Arlesheim, Switzerland.
[peter.zunker@wegmanklinik.ch] Accepted for publication April
2002.

570 Neurological Research, 2002, Volume 24, September

2£10 IE oxytocin on days 1, 4 and 5 post-partum. Blood
pressure values were in the range of 100 to 120 mmHg
systolic and 60 to 80 mmHg diastolic. Four days after
delivery, the patient complained of severe throbbing
frontal headache. On the eighth day, blurred vision
occurred, followed by three generalized tonic–clonic
seizures within 4 h. Neurological examination revealed
a somnolent woman, without focal neurological signs.
Lumbar puncture revealed a normal cerebrospinal uid.
White blood cell count, hematocrit, platelets, electrolytes and coagulation status were normal. No evidence
of collagen disorders, Wegner’s or Sjögren’s disease was
disclosed on extensive laboratory tests. The patient was
treated with Aspirin 100 mg day ¡1 and Neurontin
1200 mg day¡1 for eight and 12 weeks, respectively.
Somnolence and headache subsided within four days
after the seizures. Slowness of the movements and
cognitive function persisted for about three weeks. No
further seizures occurred and no focal signs were
observed during this period.
TCD (Multi Dop-X, DWL, Sipplingen, Germany) at the
day of the seizures showed a segmental ow acceleration in the right posterior and a disturbed ow pattern
with low frequency components in the right anterior
cerebral artery, indicating a stenotic process. The vessels
were evaluated over their whole detectable length, i.e.
the middle cerebral artery (MCA) in a depth of 35–
65 mm, the anterior cerebral artery (ACA) in a depth of
55–70 mm, and the posterior cerebral artery in a depth
of 55–70 mm, while the internal carotid arteries (ICA)
# 2002 Forefront Publishing Group
0161–6412/02/060570–03

Post-partum cerebral angiopathy: Peter Zunker et al.

Figure 1 A: Patchy hyperintense lesions in the FLAIR-sequence at day 2 after the seizures (open arrows). B: Diffusion-weighted imaging at the same
day reveals multi-focal hyperintense areas indicating increased diffusion (open arrows). C: MR-angiography (day 2) with multi-segmental narrowing of
the cerebral arteries (arrows). Magnetic resonance imaging was performed on a 1.5-T whole body scanner (Magnetom Vision, Siemens, Erlangen,
Germany), using a circular polarised head coil. Technical data: Turbo-Flair sequence with (TR 9000 msec, TE 119 msec, TI 2470 msec; matrix
154£256, FOV 165£220 mm, TA 3 : 27 min, ETL 11). Images were obtained with a slice thickness of 6 mm without interleave. Isotropic diffusionweighted images (single-shot EPI; diffusion gradients in six orthogonal directions with effective gradient amplitude of 14 mT/m; TR 6000 msec, TE
108 msec, FOV 400£200 mm; matrix 256£128; slice thickness 6 mm with 1 mm gap; 1 NEX; b value of 1221 sec/mm2 ) were applied to identify areas
of increased diffusion. Setting of the three-dimensionaltime of ight (3D-TOF) MRA: TR 35 msec, TE 7.2 msec, ip angle 20° ; matrix 200£512; FOV
150£200 mm; slab thickness 36 mm, 24 partitions; effective slice thickness 1.5 mm; TA 6 : 44 min. TR, repetition time; TE, echo time; FOV, Želd of
view; TA, time of acquisition; TI, inversion time; ETL, echo train length

Table 1: Development of the Vm ea n values in the repetitive TCD examinations at the different days after the seizures

MCA Right
Left
(Vm ea n ) [cm/sec]
ACA Right
Left
(Vm ea n ) [cm/sec]
PCA Right
Left
(Vm ea n ) [cm/sec]
ICA Right
Left
(Vm ea n ) [cm/sec]

Day 1

Day 11

Day 17

Day 20

Day 27

Day 48

95
80

110
140

110
130

90
80

90
90

80
90

50
40

140
85

120
80

100
90

90
80

80
75

70
30

96
92

85
84

30
35

30
35

30
28

45
44

46
45

48
48

48
46

45
45

44
45

MCA, middle cerebral artery; ACA, anterior cerebral artery; PCA, posterior cerebral artery; ICA, internal carotid artery.

were insonated from the submandibular approach in a
depth of 50–60 mm. MRI one day after the seizures
revealed infra- and supratentorial patchy hyperintensities in T2- and FLAIR-sequence (Figure 1A). Diffusionweighted MR revealed corresponding multi-focal hyperintense areas (Figure 1B). No contrast enhancement was
seen. Venous-phase MRA was normal. MRA of the
intracerebral arteries conŽrmed the TCD Žnding and
further disclosed a multisegmental narrowing of the
distal basal arteries (Figure 1C) MRI 10 days later
including the FLAIR-sequence was completely normal,
while a stenosis in the right M2-segment and in the right
PCA were evident on MRA. The development of the
intracranial ow velocities is displayed in Table 1. A

mild ow acceleration in all basal arteries was observed
10 days after the seizures on TCD. Elevated ow
velocities extended over the whole detectable length
of the insonated arteries and were no longer conŽned to
speciŽc segments.
Initial EEG examination disclosed a paroxysmal
dysrhythmia with sharp theta 4/s and delta 3/s with an
accentuation over the occipital and frontal lobes. Sharpwave patterns were detected in these areas under
hyperventilation. EEG was performed at time interval
of 7 to 14 days for three months. The epileptic features
disappeared after three weeks, but a theta focus
persisted over the occipital lobes. EEG normalized after
six weeks.
Neurological Research, 2002, Volume 24, September 571

Post-partum cerebral angiopathy: Peter Zunker et al.

DISCUSSION
To the best of our knowledge, this is the Žrst description
of diffusion-weighted MR imaging, repetitive TCD
examinations, and EEG follow-up examinations in a
patient with PCA. The main common feature of our
observations with earlier case reports is the Žnding of a
reversible wide spread segmental narrowing of the
intracranial arteries1,2,4,5 . Vascular narrowing in the
presented case was suggested by the initial TCD
examination and conŽrmed by MR-angiography. However, TCD underestimated the extent of the vascular
narrowing, as it is unable to evaluate the distal branches
of the basal cerebral arteries. Corresponding to the
multi-segmental narrowing of the vessels, diffusionweighted MRI revealed multi-focal hyperintensities,
indicating increased diffusion and most probably reecting cytotoxic edema due to cerebral ischemia. Repeated
MRI inclusive diffusion-weighted images at day 10 after
the seizures disclosed normal Žndings, whereby MRA
showed an improved but still ongoing occlusive vascular
process. This indicates that the angiopathy was still
present, even when brain parenchyma appeared normal.
At that time and also one week later, TCD revealed the
highest Vm e an values, most probably reecting a reactive
hyperperfusion6 . Our assumption of a reactive hyperperfusion is based on the fact that the elevation of the
ow velocities involved all basal arteries over their
whole insonable length with an increase of Vm e an also in
both ICAs, a Žnding which is incompatible with
segmental narrowing. An ongoing pathological process
was also documented in the repetitive EEG examinations, which only normalized after six weeks of antiepileptic treatment indicating that irregular brain function in PCA still exists when brain parenchyma appears
normal in imaging studies.
The term PCA reects an intracranial vessel narrowing
of unclear etiology. While most authors interpret it as
vasospasm1,4,5 some discuss a form of benign vasculitis
conŽned to the cerebrum7 ,8 or a hormonally induced
intima hyperplasia9 . A higher susceptibility of the brain
vessels to various drugs (including sympathomimetics2 ,
lisuride3 , ergot alkaloids and derivates5,7,10 and sumatriptan1 0 ) as a consequence of an altered post-partum
hormonal stage has also been proposed1 0 . Finally,
earlier reports have argued for immunological and
biochemical mechanisms triggering this angiopathy
due to remaining placental tissue in the uterus11,12 . So
far, even one autopsy study cannot clearly contribute to
the pathophysiology of PCA, as a slight intimal thickening and a disruption of the elastic lamina of the brain
vessels were the only pathological Žndings4 .
In the present case drugs did not play a causative role.
Oxytocin, which was repetitively used, has no immediate vascular effect, since in the arteries its receptors are
lacking1 3 . Remaining placental tissue after the delivery
of twins in the presence of an atonic uterus is the only
potential pathogenic mechanism in the present case.
Since PCA is not clearly deŽned, patients with the
same disease may be summarized under different
diagnoses. These include late onset post-partum eclampsia1 1,12 , isolated vasculitis of the brain in pregnancy and
572 Neurological Research, 2002, Volume 24, September

puerperium14 , post-partum cerebral angiopathy1– 3,5 ,
and delayed peri-partum vasculopathy8 . Related to
these different diagnoses and pathophysiological considerations, different therapeutic regimes have been
applied. These included corticosteroids3,5 ,7 ,9 , cyclophosphamid14 , nimodipine15 , heparin5 , and hypervolemic agents1 6 . Diphenylhydantoin is mostly chosen as
anti-epileptic drug. We treated our patient with Aspirin
and Neurontin only, and observed an uneventful clinical
course. Obviously, no therapeutic conclusions can be
drawn from this case report, but we believe that
combined use of antiplatelet and anti-epileptic agents
should be considered, particularly in view of the
potential complications of some of the agents currently
applied for treatment of PCA.
CONCLUSION
Our presented case of PCA provides a better insight into
the pathophysiology of this intriguing disease. TCD and
EEG may be the appropriate means to determine the real
conclusion of the disease. The uneventful clinical course
under our therapeutic regime merits further evaluation.
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