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Delayed peripartum vasculopathy Cerebral eclampsia revisited.

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Although motor cortex normally contains slightly
higher amounts of iron compared to other parts of the
cerebral cortex [9f, this difference seems too subtle to
produce the observed difference in signal intensities
on MRI. In fact, there was no difference in signal intensities between motor cortex and other cortices in the
control patients. However, primary degeneration of
motor cortex [lo, 111 might allow iron to accumulate
in this area, and thus produce the signal loss on MRI.
To our knowledge, there are no neuropathological
investigations or quantitative analyses of iron in motor
cortex of patients with ALS. Further studies are
needed. Nevertheless, signal loss in motor cortex in
ALS might specifically reflect primary upper motor
neuron involvement of this disease.
This work was supported in part by a grant from the Tokyo Metropolitan, Institute of Gerontology.
We are very grateful to Drs Yasuoki Mashima (Tokyo Metropolitan
Geriatric Hospital) and Hidehiro Mizusawa (University of Tsukuba)
for their helpful comments and encouragement o n this study.
~~
References
1. Goodin DS, Rowley HA, Olney RK. Magnetic resonance imaging in amyotrophic lateral sclerosis. Ann Neurol 1988;23:
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2. Sales Luis ML, Hormigo A, Mauricio C, er al. Magnetic cesonance imaging in motor neuron disease. J Neurol 1990;237:
47 1-474
3. Iwasaki S, Nakagawa H, Fukusumi A, et al. Identification of
pre- and posrcentral gyri on CT and MR images on the basis
of the medullary pattern of cerebral white matter. Radiology
1991;179:207-2 13
4. Oba H, Araki T, Monzawa S, et al. MR imaging of amyotrophic
lateral sclerosis. Nippon Acta Radio1 1992;52:427-435
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93
6. Rutledge JN, Hilal SK, Silver AJ, et
7.
8.
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10.
11.
al. Study of movement
disorders and brain iron by MR. AJR 1987;149:365-379
Harrison WW, Netsky MG, Brown MD. Trade elements in
human brain: copper, zinc, iron, and magnesium. Clin Chim
Acta 1968;Z1:5 5 -60
Runge VM, Clanton J A , Smith FW,et al. Nuclear magnetic
resonance of iron and copper disease states. AJR 1983;141:
943-948
Hallgren B, Sourander P. The effect of the age on the nonhaemin iron in the brain. J Neurochem 1958;3:41-51
Oppenheimer DR. Diseases of the basal ganglia, cerebellum and
motor neurons. In: Adams JH, Corsellis JAN, Duchen LW,
eds. Greenfield’s neuroparhology. 4th ed. New York: Wiley,
1984699-747
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system in motor neuron disease.J Neurol Neurosug Psychiatry
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Delaved Peritxrtum
Vasculopath< Cerebral
Eclampsia Revisited
Eric C. Raps, MD,” Steven L. Galetta, MD,”
Magie Broderick, BA,” and Scott W. Atlas MDI
Over a 2-year period, we treated 4 postpartum patients
with acute neurologic problems appearing 4 to 9 days
after delivery. Three patients either had no proteinuria
or edema and therefore did not meet all accepted clinical
criteria for the diagnosis of eclampsia. Magnetic resonance imaging (MRI) of the brain in all patients demonstrated high-signal foci most prominent in the parietooccipital regions and the subcortical white matter.
Cerebral angiogram in 2 patients revealed diffuse vasospasm. In 3 patients, MRI abnormalities resolved. MRI
and angiographic abnormalitiesin our patients are identical to those of patients meeting accepted criteria for
eclampsia. Our experience suggests that the current criteria for the diagnosis of eclampsia are too stringent,
both in terms of clinical picture and days postpartum to
cerebral manifestations.
Raps EC, Galetta SL, Broderick M, Atlas SW.
Delayed peripartum vasculopathy: cerebral
eclampsia revisited. Ann Neurol 1993;33:222-225
Eclampsia is defined by the concurrence of proteinuria,
edema, hypertension, and convulsions or coma in the
intrapartum or immediate postpartum period [I, 27.
Several factors have been proposed to explain the spectrum of neurological signs and symptoms observed in
this disorder, including cerebral vasospasm, microhemorrhage, ischemia, and hypertensive encephalopathy
[3-91. Current clinical definitions impose a postpartum
“time limit” of 2 days on eclampsia as an explanation
for neurological deterioration after delivery [l, 21, although this time period has been controversial [ S , 61.
Magnetic resonance imaging (MRI) has been useful in
defining a predictable neuroradiological appearance of
cerebral eclampsia, most notably transient bilateral parietooccipital high-signal intensity involving cortex and
subcortical white matter [lo- 13f.
Over a 24-month period, we encountered 4 postpartum women with acute neurological problems that occurred 4 or more days following delivery. Although all
From the Departments of ‘Neurology and *Radiology, Hospital of
the University of Pennsylvania, Philadelphia, PA.
Received Jun 19, 1992, and in revised form Aug 27 and Sept 10.
Accepted for publication Sept 10, 1992.
Address correspondence to D r Raps, Department of Neurology,
Hospital of the University of Pennsylvania, 3400 Spruce Sr, Philadelphia, PA 19104.
222 Copyright 0 1993 by the American Neurological Association
4 patients had similar MRI abnormalities, their clinical
presentations were not similar, and 3 patients did not
have edema, proteinuria, or both.
Methods
Three of the 4 patients were seen by us (E.C.R. and S.L.G.).
To put this experience in context, we reviewed the charts of
women with acute neurological postpartum complaints presenting to the Hospital of the University of Pennsylvania in
1990 and 1991. We identified 9 patients in whom seizures,
mental status changes, or focal neurologic deficits developed
more than 3 days following delivery. We chose a 3-day lower
limit because many authorities [I, 2) have defined 48 hours
as an interval beyond which cerebral eclampsia is considered
unusual or improbable. Four patients were known to have
epilepsy and were excluded. One other patient was excluded
after serological tests were consistent with systemic lupus
erythematosus. The remaining group of 4 patients-all without prior neurological conditions-had MRI scans at the onset of symptoms and again 2 weeks (1 patient), 12 weeks (2
patients), and 1 year ( 1 patient) later.
MRI was performed on a 1.5-T Signa Scanner (General
Electric, Milwaukee, WI) using conventional spin-echo techniques. T1-weighted images were obtained using a long TR
sequence (TR = 2,700-3,000 msec) with short TE (TE <
40 msec) and long TE (TE > 80 msec). Two patients also
underwent intraarterial catheter arteriography 36 to 48 hours
following ictus.
Illustrative Case Report (Patient 2)
Preeclampsia developed in a 24-year-old gravida 5,
para 3 at 36 weeks’ gestation. She was delivered by
cesarean section and her blood pressure normalizied.
She remained well until the fourth postpartum day,
when she noted severe headache and “blurry vision.”
Examination revealed a blood pressure of 160/110 and
cortical blindness. MRI demonstrated multiple areas
(Figure A, B) of increased signal intensity in the occipital lobes bilaterally (greater on the left than right) involving both cortical and subcortical regions. She was
treated with antihypertensives, and her vision returned
to normal by the eighth postpartum day. One year
later, a follow-up MRI scan of the head was normal
(Figure C , D).
Results
Seizures developed in 3 patients and cortical blindness
developed in 1 patient 4 days or more following delivery. Clinical information is summarized in the Table.
Parietooccipital or occipital high-signal abnormalities
were seen on MRI in all patients and completely resolved in 3. Pelvic examinations were unrevealing in
all patients.
Discussion
We describe 4 postpartum patients with MRI and angiographic findings typical of cerebral eclampsia but in
whom all clinical criteria for the syndrome were not
present. The American Congress of Obstetricians and
Gynecologists [1) and William’s Obstetrics { 2 } continue
to define the window of postpartum eclampsia (PPE)
as less than 2 days with rare exceptions. Stander and
colleagues 114) argued to extend the postpartum
eclamptic period from 24 hours to 6 days in their report of eclampsia occurring on postpartum days 4, 6,
and 8, and Samuels Cl51 concluded that cerebral
eclampsia can occur within a few minutes or as late as
23 days (1 patient) after delivery. Despite these and
other similar reports {S, 61, the accepted time limit on
PPE remains within 48 hours.
The 4 patients we describe demonstrated late onset
of cerebral symptoms, lack of fulfillment of the preeclamptic triad (3 patients lacked proteinuria, edema,
or both), and marked variation in severity of neurological signs and symptoms; however, the appearance of
their MRI was remarkably uniform and matched previous descriptions of MRI in patients with classic eclampsia. Certain organ systems or vascular beds may be
especially susceptible to eclampsia; the brain is perhaps
most vulnerable of all [l6]. The MRI changes observed
in our patients were consistent with ischemia or edema
principally affecting subcortical white matter of the parietooccipital region.
The pathophysiology of cerebral eclampsia remains
unclear, although important comparisons have been
made with hypertensive encephdopathy-an
entity
with a similar MRI appearance [17]. McAlpine [I81
first postulated that acute elevations in mean arterial
pressure exceeded capillary resistance and resulted in
cerebral edema. In 1902, Bayliss [191 demonstrated
that arterial muscle has an intrinsic tone governed by
intraarterial tension. He suggested that encephalopathy
ensues when arterial spasm is stimulated by elevated
intraarterial tension. Byrom [4] emphasized Bayliss’
earlier findings and used a rat experimental model to
demonstrate the role of arterial spasm in the pathogenesis of cerebral injury seen in both eclampsia and hypertensive encephalopathy. Angiograms in patients
with PPE have shown segmental narrowing consistent
with vasospasm or a “rapidly resolving” isolated vasculitis {7-9). Cunningham and Lindheimer [20], in a recent review of hypertension in pregnancy, suggested
prostaglandin deficiency or endothelial-cell dysfunction
as potential causes for altered vascular reactivity in preeclampsia.
MRI studies in patients with intrapartum and postpartum eclampsia consistently [10- 131 reveal hyperintensive foci concentrated in the parietooccipital
regions. Duncan and colleagues [13] reported 3 patients with cortical blindness complicating eclampsia
and “reversible” ischemic occipital lesions seen on
MRI. Patients meeting accepted clinical criteria for cerebral eclampsia and postpartum patients with neuro-
Brief Communication: Raps et al: Delayed Peripartum Vasculopathy
223
A
R
C
D
Axial T2-weighted MRI. (A, B) Initial MRI demonstrates bilateral parietooccipital high-signal intensity abnormalities in
the subcortical whire nratter. (C, 0)Resolution of abnormalities
on follow-up MRI 1 year later.
Patient Characteristics
No.
Age
(yr)
GraviddPara Hypertension Proteinuria Edema Presentation Day of Onset MR1 Results
1
14
'110
+
-
-
HIA, seizures
4
Bilateral parierooccipital and temporooc-
2
24
'513
+
+
+
HIA, cortical blind-
4
3
36
'212
+
-
-
Seizures
7
Patient
4
+
40
=
Postpartum
'211
NA
Negative (12 weeks)
Occipital high signal
NA
Negative ( 1 year)
Posterior parietal high
Vasospasm Negarive ( I 2 weeks)
cipiral high signal
ness
+
+
positive; - = negative; NA
Angiogram Follow-up
MRI Results
Results
=
signal
HIA, seizures
9
Bilateral parietooccipital h g h signal
Vasospasm
Positive for anterior cerebral artery infarction ( 2 weeks)
not applicable
logical deficits, like those reported herein, display
similar MRI and angiographic appearances. These characteristic neuroradiologic changes may be observed
even in the absence Of proteinuria Or edema' Vasespasm, possibly precipitated by elevated intraarterial
pressure, has a prominent role in subsequent cerebral
ischemia, which is often, but not always, reversible. We
propose that the definition of eclampsia be expanded
to encompass this diverse g o u p Of patients with unifying underlying pathophysiology.
References
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CT: Appleton and Lange, 1989653-694
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AJNR 1989;10:445
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13. Duncan R, Hadley D, Bone I, et al. Blindness in eclampsia CT
and MR imaging. J Neurol Neurosurg Psychiatry 1989;52:
899-902
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eclampsia. Am J Obstet Gynecol 1946;52:765-772
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748-752
16. Lewis LK, Hinshaw DB, Will AD, et al. CT and angiographic
correlation of severe neurological disease in toxemia of pregnancy. Neuroradiology 1988;30:804-806
17. Hauser RA, Lacey M, Knight MR. Hypertensive encephalopathy: MRI demonstration of reversible cortical and white matter
lesions. Neurology 1988;38(suppl 1):llO
18. McAlpine D. The hypertensive cerebral attack. Q J Med
1933;2:463-481
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of internal pressure. J Physiol 1902;28:220-23 1
20. Cunningham FG, Lindheimer MG. Hypertension in pregnancy.
N Engl J Med 1992;326:927-932
Brief Communication: Raps et al: Delayed Peripartum Vasculopathy
225
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