PEDIATRICS Vol. 100 No. 4 October 1997,
p. e8
Copyright ©1997 by the American Academy of Pediatrics
ELECTRONIC ARTICLE:
An Unusual Cause of Neonatal Seizures in a Newborn Infant
O. L. de Klerk
T. W. de Vries
Department of Pediatrics
Leeuwarden Medical Centre
Leeuwarden, The Netherlands
L. G. F. Sinnige
Department of Neurology
Leeuwarden Medical Centre
Leeuwarden, The Netherlands
ABSTRACT
- INTRODUCTION
- CASE REPORT
- COMMENTS
- ABBREVIATIONS
- REFERENCES
ABSTRACT 
Neonatal seizures in the neonatal period are symptoms of
numerous underlying disorders of the neonate. We present a case in which neonatal seizures due to cerebral infarction led to a diagnosis in the mother.
Neonatal convulsions caused by cerebral artery thrombosis is relatively
rare in the neonatal period and is often secondary to indwelling
intravascular catheters that cause thromboembolism, but may be
associated with many conditions.1
Cerebral artery thrombosis in newborns, in which antiphospholipid
antibodies (APA) were found in the mother, has been described in three
case reports.2,3 Two of these premature infants were born
with other risk factors for thrombosis. APA could not be identified in
any of these three infants. In the two cases reported by Silver et
al3 the diagnosis was made several months after birth.
This case is unique in the fact that no other risk factors for
thrombosis could be identified to explain the infarction, and that APA
were found in the offspring of an apparently healthy mother. Whether
the prior fetal death was caused by APA remains unclear. The finding of
lupus anticoagulant in her child led to the diagnosis of
antiphospholipid antibody syndrome in her. We believe that in case of
cerebral artery thrombosis in a neonate, with no trivial cause such as
an indwelling catheter or sepsis, both mother and infant should be
tested for presence of APA, even when the mother seems
healthy.
Key words:
neonate,
cerebral infarction,
maternal
antiphospholipid syndrome.
INTRODUCTION
Neonatal seizures in the neonatal period are symptoms of
numerous underlying disorders of the neonate. We present a case in which neonatal seizures due to cerebral infarction led to a diagnosis in the mother.
CASE REPORT
A 3-day-old male infant was referred to the
neonatology ward because of convulsions. He was born at 39-weeks
gestation, after a normal vertex delivery. His 25-year-old mother had a
history of one intrauterine fetal death at 20 weeks. This pregnancy had been uncomplicated, although his mother had noticed numerous periods of
subtle movements in the last 4 weeks of her pregnancy that felt
different from normal fetal movements or uterine contractions and never
lasted more than 2 minutes. The infant weighed 3500 g (P50), was
54 cm long (P90), and had a head circumference of 35 cm (P50). A few
hours after birth, he started to have multiple subtle seizures
manifested by repetitive blinking, smacking movements, right-sided
twitching of the head and ipsilateral hand and foot. None of the
seizures lasted more than 3 minutes. Neurologic examination was
otherwise normal. Hematological evaluation, glucose, and electrolytes were normal. There were no signs of an intrauterine infection. An
electroencephalogram showed an intermittent irritative disturbance in
the left hemisphere.
An ischemic left-middle cerebral artery infarct with a minor hemorrhage
could be identified on magnetic resonance imaging (MRI) (Fig
1). On additional magnetic resonance
angiography no vascular aberrations of the large vessels were seen.
Duplex of the carotid arteries and transcranial Doppler did not show
any abnormalities. Coagulation studies revealed lupus anticoagulant (LAC) immunoglobulin G (IgG) presence, the titer being 18.9 GPL units/mL (normal 
10 GPL units/mL). Anticardiolipin antibody was negative. Detection of LAC and anticardiolipin IgG was performed according to the methods described by Brandt et al.1
Activated partial thromboplastin time and prothrombin time were both
normal. Protein S, protein C activity, and antithrombin III-activity
were normal for age. Factor VLeiden was absent. An
electrocardiogram showed no signs of heart blockage. His mother was
additionally tested (6 days later) for antiphospholipid antibodies
(APA) and she seemed to have an anticardiolipin IgG titer of 20 GPL
units/mL (normal 10 GPL units/mL); LAC was negative.
Fig. 1.
MRI image of the brain made 1 week postpartum showing edema of the left
hemisphere with a small hemorrhage, corresponding with a left middle
cerebral artery infarction.
[View Larger Version of this Image (112K GIF file)]
The child was given phenobarbital on day 4. The convulsions were not
seen after day 5, and no other problems were encountered. He was
discharged on day 8, and is still doing well. After 1 month, he became
LAC-negative. At the age of 3 months, the MRI showed an old infarct of
the left middle cerebral artery with some cortical atrophy (Fig
2). At neurologic examination at the age of 1 year, no asymmetry in motor function was found and there were no signs of developmental delay.
Fig. 2.
MRI image made at 3 months after birth showing focal cortical atrophy
of the left parietal lobe, suggesting an old infarction of the left
middle cerebral hemisphere.
[View Larger Version of this Image (122K GIF file)]
COMMENTS
In the neonatal period, convulsions are mostly attributable
to perinatal asphyxia, metabolic derangements, or
infections.2 Thromboembolism is a relatively rare
cause of convulsions in the newborn and is often secondary to
indwelling intravascular catheters,3 but may be associated
with many conditions. Thromboembolism in newborns of LAC-positive
mothers has been described.4,5 Affected women
characteristically have poor pregnancy outcomes that may be improved
with prednisone and low-dose aspirin treatment.6 Zurgil7 showed transplacental transfer of APA in 18 pregnant women, but in none of the cases could clinical manifestations of APA syndrome be detected. Titers of APA in affected women may fall
after pregnancy. This may explain why anticardiolipin antibodies, and
not LAC, could be detected in the mother at the time of determination.
Cerebral artery thrombosis in newborns, in which APA were found
in the mother, has been described in three case reports.8,9 Two of these premature infants were born with other risk factors for
thrombosis. In none of the three cases could APA be identified in the
infant. In the two cases reported by Silver et al9 the diagnosis was made several months after birth.
This case is unique in the fact that no other risk factors for
thrombosis could be identified to explain the infarction and that APA
were found in the offspring of an apparently healthy mother. Whether
the prior fetal death was caused by APA remains unclear. The finding of
LAC in her child led to the diagnosis of antiphospholipid antibody
syndrome in her. This is comparable with diagnosing systemic lupus
erythematosus in mothers of children with Ro-SSA positive congenital
heart block or neonatal thrombocytopenia.10
We believe that in the case of thromboembolism in a neonate, with no
trivial cause such as an indwelling catheter or sepsis, both mother and
infant should be tested for the presence of APA, even when the mother
seems healthy.
FOOTNOTES
Received for publication Dec 2, 1996; accepted Feb 15, 1997.
Reprint requests to (T.W.d V.) Department of Pediatrics,
Medisch Centrum Leeuwarden, Mr PJ Troelstraweg 78, 8917 CD Leeuwarden,
The Netherlands.
ABBREVIATIONS
MRI, magnetic resonance imaging.
LAC, lupus
anticoagulant.
IgG, immunoglobulin G.
APA, antiphospholipid antibodies.
REFERENCES
-
Brandt JT,
Barna LK,
Triplett DA
Laboratory identification of
lupus anticoagulant: results of the second international workshop for
identification of lupus anticoagulant.
Thromb Haemost.
1995;
74:1597-1603[Medline]
-
Hill A, Volpe JJ. Neurologic disorders. In: Avery GB, Fletcher MA,
MacDonald MG, eds. Neonatology: Pathophysiology and Management of
the Newborn. 4th ed. Philadelphia, PA: JB Lippincott Company;
1994:1119-1120
-
Kotlarek F,
Thron A,
Weber U,
Der Schlaganfall beim Kind:
Ätiologie, Differentialdiagnose, sinnvolle Diagnostik und
therapeutische Möglichkeiten.
Klin Padiatrie
1993;
205:332-339
-
Sheridan-Pereira M,
Porreco RP,
Hays T,
Neonatal aortic
thrombosis associated with the lupus anticoagulant.
Obstet
Gynecol.
1988;
71:1016-1018[Abstract/Free Full Text]
-
Finazzi G,
Cortelazzo S,
Viero P,
Maternal lupus anticoagulant
and fatal neonatal thrombosis.
Thromb Haemost.
1987;
87:238
-
Lubbe WF,
Butler WS,
Palmer SJ,
Lupus anticoagulant in
pregnancy.
Br J Obstet Gynaecol.
1984;
91:357[Medline]
-
Zurgil N,
Bakimer R,
Tincani A,
Detection of anti-phospholipid
and anti-DNA antibodies and their idiotypes in newborns of mothers with
anti-phospholipid syndrome and SLE.
Lupus
1993;
2:233-237[Abstract/Free Full Text]
-
Tabbut S,
Griswold WR,
Ogino, MT, et al
Multiple thrombosis in a
premature infant associated with maternal phospholipid antibody
syndrome.
J Perinatol.
1994;
14:66-70[Medline]
-
Silver RK,
MacGregor J,
Pasternak JF,
Fetal stroke
association with elevated anticardiolipin antibodies.
Obstet
Gynecol.
1992;
80:497-499[Medline]
-
Esscher E,
Scott JS
Congenital heart block and maternal systemic lupus
erythematosus.
Br Med J.
1979;
1:1235
