Focal Motor Seizures Heralding Stroke
in Full-term Neonates
Robert Clancy, MD; Seth Malin, MD; Danielle Laraque, MD; Stephen Baumgart, MD; Donald Younkin, MD
\s=b\ We describe the clinical syndrome,
medical management, etiology, and neurologic outcome of stroke diagnosed by
computed tomographic scan in 11 fullterm neonates encountered during a
two-year period. Neonatal stroke is relatively common and may appear in the
setting of diverse cerebrovascular disorders such as hypoxic-ischemic enceph-

alopathy, polycythemia, acute severe
hypertension, and embolization. Repetitive, persistently unifocal motor seizures heralded localized cerebral injuries in eight infants. The majority of
patients did not display any other lateralized clinical neurologic signs. An electroencephalogram revealed a focal or
lateralized functional central

nervous

system abnormality in ten cases. All of

the initial computed tomographic scans
were focally abnormal. However, cranial
ultrasound examinations were insensitive to stroke in nine patients. Medical
management included careful cardiorespiratory support, correction of coexist-

ing metabolic or system abnormalities,

and aggressive administration of anticonvulsants to promptly eliminate seizures. Limited follow-up suggests that
many affected infants may enjoy favorable outcomes.

(AJDC 1985;139:601-606)
Tocalized nontraumatic cerebral in¬
farction is infrequently diagnosed
antemortem in the term neonate.1"4
Diffuse encephalopathy is more preva¬
lent, encountered secondary to global
From the Divisions of Neurology (Drs Clancy
and Younkin), Neonatology (Drs Malin and
Baumgart), and General Pediatrics (Dr Laraque), The Children's Hospital of Philadelphia;
and the Departments of Neurology (Drs Clancy
and Younkin) and Pediatrics (Drs Clancy, Malin,

Laraque, Baumgart, and Younkin), The University of Pennsylvania School of Medicine, Phila-

delphia.
Reprint requests to Division of Neurology, The
Children's Hospital of Philadelphia, 34th Street
and Civic Center Boulevard, Philadelphia, PA
19104 (Dr Clancy).

cerebral injuries such

birth as¬
phyxia5
hypoglycemia. Whereas
much attention has been focused on
the neurologic characteristics and
prognosis of the more common diffuse
cerebral hypoxia-ischemia, no detailed
report has described the simultaneous
clinical, neuroradiologic, and electroencephalographic (EEG) correlates
and neurologic sequelae of localized
cerebral infarction. The clinical recog¬
nition of neonatal stroke has been ham¬
pered by the low frequency of associ¬
ated lateralized neurologic signs1,3 and
the wide recognition that focal motor
seizures in the term neonate do not
necessarily indicate an underlying
discrete structural central nervous
system (CNS) lesion. As a result, no
general approach for the detection,
diagnostic evaluation, medical man¬
agement, and neurologic prognosis of
neonate stroke has emerged.
The purpose of this report is to de¬
lineate the clinical syndrome, medical
management, etiology, and prognosis
of neonatal stroke by describing 11
term neonates with localized cerebral
infarction confirmed by computed to¬
mographic (CT) scan. The infants typ¬
ically presented with a cerebrovas¬
cular disorder heralded by repetitive,
persistently unifocal motor seizures
and definite focal EEG abnormalities
but no lateralized abnormality of
clinical neurologic and cranial ultra¬
sound examinations.
as

or

PATIENT REPORTS
Eleven consecutive full-term infants with
CT scan-verified localized cerebral infarc¬
tion were evaluated by the authors during a
24-month period at three affiliated inten¬
sive care nurseries in a large metropolitan
area. The cases are summarized in the
Table. Three representative patients are
described below.

Patient 1.—A 3.0-kg female infant was
the product of a full-term gestation compli¬
cated only by maternal smoking. Apgar
scores were 8 and 9 at one and five minutes,
respectively, and results of the newborn
physical examination were normal. A
screening hematocrit determination at the
age of 12 hours was 71% and a repeated
value at 28 hours was 67%. The infant was
orally hydrated and appeared well until her
first focal seizure at 48 hours of age. Re¬
sults of extensive testing for metabolic ab¬
normalities, intoxication, and sepsis were
normal. Blood viscosity was 18 centipoise
(normal values, 6 to 9 centipoise at a shear
rate of 10 s1). A partial exchange transfu¬
sion reduced her hematocrit and blood vis¬
cosity to normal. Cerebrospinal fluid, cran¬
ial ultrasound examination results, and an
echocardiogram were normal. Her EEG
revealed voltage attenuation and the ab¬
sence of a normal transient, encoche fron¬
tale, in the left frontal area. A CT scan
obtained 18 hours after the first seizure
revealed a discrete lucency in the left lat¬
eral-frontal cortex. She experienced re¬
peated focal seizures characterized by
coarse clonic jerking of the right arm and
leg and conjugate ocular deviation to the
left. Neurologic examination disclosed in¬
activity, lethargy, and hypotonia but no
persistent lateralized signs. A mild postic¬
tal right hemiparesis lasted 12 hours. A
follow-up CT scan at the age of 3 months
showed a persistent stroke (Fig 1). She was
neurologically and developmentally normal
at 17 months of age.
Patient 6.—A 4.2-kg male infant was
the product of an uncomplicated full-term

gestation to a healthy primigravid 17-yearold woman. Three hours prior to delivery,

severe variable fetal heart rate decelera¬
tions were observed and meconium was
passed. The one-minute Apgar score was 1
and he required vigorous resuscitation in
the delivery suite. On the first day of life, he
was stuporous, inactive, and hypotonie.
His eyes were briefly deviated conjugately
to the left but no other lateralized clinical
abnormalities were present. Subtle and
focal right-sided tonic seizures were recog-

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Clinical, EEG, and Radiologie Findings in 11 Infants With Focal Cerebral Injuries*
Patient/Apgar

Coexisting

Scores (1 and
5 min) Birth

Metabolic
Neurologic
Abnormalities
Examination
Weight, kg
Etiology
Focal motor
1/(8 and 9)/3.0 Polycythemia, None
hyperviscosity
seizures,

lethargy,

transient right

EEG
Absent left-sided
encoche

frontale, voltage

Cranial
Ultrasound
Normal

(day 1)

CT Scan

Outcome

Left lateral frontal Normal at 17 mo
infarction (day 1)

attenuation

hemiparesis,
hypotonia

2/(8 and 9)/3.5 Polycythemia

3/(5 and 7)/3.9 Postpartum

ischemia from
acute blood
loss

4/(1 and ?)/3.1 Intrapartum
asphyxia

5/(4 and 7)/3.3 Intrapartum
asphyxia

6/(1 and 5)/4.2 Intrapartum
asphyxia

Focal motor

None

seizures, normal

Hypoglycemia
(seizures
persisted after
correction)

None

interictal
examination
results
Focal motor

seizures,

lethargy,
inactivity,
hypotonia,
subtle right
hemiparesis
Focal motor

seizures,

lethargy,
inactivity,
hypotonia

Hypoglycemia Focal motor
(seizures
seizures,
persisted after lethargy,
correction)
inactivity,
hypotonia
None

Focal slowing,

sharp waves,
seizures right
central region

Persistently

attenuated
voltage of left

central-temporal
regions

Electrographic

seizures
confined to left

hemisphere
Electrographic

seizures
confined to right

Normal (days
2 and 7)

paresis

Normal at 24 mo

right artery
(day 2)
Infarction left

Normal

(day 3),
generalized
edema

temporoparietal
areas (day 4)

(day 8)
Generalized
edema
(day 1 )

Infarction of left

multifocal onset
seizures (mostly
from left

Right
hemiparesis,
developmental
delay at 17 mo

Normal at 17 mo

temporoparietal
area (day 3)

Normal (days Infarction of right
1 and 7)
occipitoparietal
area

occipital-central
region
Subtle and focal Persistently
Normal
attenuated
motor seizures,
(day 2)
lethargy,
voltage of left
inactivity,
temporal region,
transient gaze

Infarction in
distribution of
middle cerebral

Normal at 8 mo

(day 2)

Infarction in
distribution of
left middle
cerebral artery

(day 5)

Survived with no
lateralized

neurologic
signs

hemisphere)

Fig 1.—Patient 1. Follow-up computed to¬
mographic scan at 3 months of age follow¬
ing neonatal polycythemia, hyperviscosity,

and right-sided focal clonic seizures shows
localized superficial infarction in left frontal
cortex in anterior distribution of middle cere¬
bral artery.

Fig 2.—Patient 10. Computed tomographic
days of age demonstrates Infarc¬

scan at 2

tion in distribution of left middle cerebral
artery. Cerebral angiography revealed em¬
bolie occlusions of trifurcation of left middle
cerebral artery and left posterior cerebral

artery.

nized clinically. Cranial ultrasound ex¬
amination results on the second day of life
were normal. His EEG was markedly ab¬
normal due to status epilepticus. Over 90%
of numerous electrographic seizures arose
from the left frontal, central, or temporal
regions. An occasional electrographic sei¬
zure appeared independently in the right
central area. The interictal EEG displayed
a striking voltage attenuation and periodic
sharp-slow waves in the left temporal area.
A phosphorus 31 nuclear magnetic reso¬
nance (NMR) spectroscopy examination
during recurrent clinical seizures revealed
a marked left hemisphere depletion of
phosphocreatine and accumulation of in¬
organic phosphates.6 Subsequent NMR
spectra did not improve until seizure con¬
trol was achieved with phénobarbital so¬
dium and phenytoin sodium. A CT scan
obtained on the fifth day of life revealed an
infarction in the distribution of the left
middle cerebral artery. No lateralized
clinical neurologic signs were observed on
hospital discharge at 2 weeks of age.
Patient 10.—A male infant was the

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Clinical, EEG, and Radiologie Findings in 11 Infants With Focal Cerebral Injuries (cont)
Patient/Apgar

Scores (1 and

Coexisting

Metabolic
Neurologic
Abnormalities
Examination
Weight, kg
Etiology
7/(9 and 10)/3.2 Hypernatremia, Hypernatremia, Focal motor
dehydration
acidosis,
seizures,
azotemia,
lethargy,
hypercalcemia inactivity,
(seizures
hypotonia
appeared after
5 min) Birth

EEG

Cranial
Ultrasound

Focal slowing and Increased

positive sharp
waves in right
temporal region

echogenicity
in right
temporal
lobe (day 2)

CT Scan

Outcome

Hemorrhagic

Normal at 22 mo

infarction, right
temporal lobe
(day 5)

metabolic

8/(8 and 9)/2.0 Acute,
prolonged
hypertension
from renal

compression
by a
mesoblastic

nephroma
9/(9 and 9)/3.7 Embolisms

correction)
Diffuse
Bioccipital
Microcephaly,
Hypoglycemia, Multifocal clonic Focal status
infarctions with
edema
developmental
hyperkalemia, seizures, coma, epilepticus in
both
and
2
azotemia,
hypotonia
(days
luxury perfusion delay at 18 mo
2
and
acidosis,
occipitotemporal 10)
(days
5)
(seizures
regions
after
persisted
correction)
None

from left atrial
wall mass
(? mural
thrombus vs
atrial myxoma)

10/(9 and 10)/4.1 Embolie

Focal motor

Normal

Normal

Normal at 20 mo

Bifrontal
infarctions

(day 3)

seizures, alert,
active, normal

(day 5)

tone

None

Focal motor

Focal slowing,

occlusions of
left posterior
and middle
cerebral
arteries from
unidentified

seizures,

sharp waves

facial

central-temporal
regions

venous
source

following

lethargy,
inactivity, mild
hypotonia, brief
asymmetry

and seizures
confined to left

Absent
vascular

Infarction in
distribution of
pulsations of left middle
left middle
cerebral artery
cerebral
(day 2)

Normal at 5 mo

artery,

compression

of left lateral
ventricle

seizures

(day 2)
11/(5 and 9)/3.2 Presumed

None

embolie
occlusion
from
unidentified

Lethargy,
inactivity, and
apnea and

bradycardia;
minimal right-

venous

sided facial

source

flattening;
congenital

Marked persistent Diffuse
edema
voltage
attenuation of
(day 1)
entire left

hemisphere

Infarction in
distribution of
left internal
carotid artery

(day 4)

Survived,

minimal rightsided facial

flattening

infarction of
right arm with

angiographically
demonstrated
subclavian
artery embolie
occlusion
*EEG indicates electroencephalography; CT, computed tomographic.

4.1-kg product of a full-term, uncompli¬
cated gestation to a healthy woman. He was
delivered by cesarean section for poor labor
progress. Apgar scores were 9 and 10 at one
and five minutes, respectively, and the
newborn physical examination results were
normal. His first right-sided focal clonic
seizure appeared at 24 hours of age. He
became mildly lethargic, inactive, and hy¬
potonie. A transient subtle facial asymme¬
try briefly followed his seizures but no
other lateralized clinical findings were ap¬
parent. Cranial ultrasound examination at
the age of 2 days revealed absent vascular
pulsations in the left middle cerebral artery
and an apparent mass effect with compres-

sion and narrowing of the width of the left
lateral ventricle. No parenchymal abnor¬
malities were noted. An EEG demon¬
strated focal slowing, sharp waves, and
several seizures confined to the left central
and temporal regions. An infarction in the
distribution of the left middle cerebral ar¬
tery was demonstrated by CT scan at 2 days
of age (Fig 2). No metabolic or cardiac
abnormalities were found. Cerebral an¬
giography revealed normal carotid arteries
and embolie occlusions of the left posterior
cerebral and the trifurcation of the left
middle cerebral arteries. He was developmentally and neurologically normal at 5
months of age.

RESULTS
Clinical Neurologic Signs of Stroke
There

were

few definite clinical

signs revealing the presence of a

stroke. Clinical seizures were ob¬
served in ten of 11 infants. Unifocal
clonic seizures were present in eight
patients, multifocal clonic in one pa¬
tient, and both subtle and unifocal
tonic seizures in another patient. In all
infants with concurrent metabolic ab¬
normalities (eg, hypoglycemia), sei¬
zures persisted despite correction of
the derangement. Clinical seizures

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underwent a follow-up CT scan ex¬
amination obtained one to three
months after the acute encephalopa¬
thy. In comparison, cranial ultrasound
examinations obtained one to ten days
after the onset of illness were fre¬
quently insensitive to stroke. Results
of all cranial ultrasound examinations
in nine patients were normal or showed
diffusely increased "echogenicity."
Even with knowledge of the CT loca¬
tion of focal injury, follow-up studies
within two weeks of the injury in four
patients failed to recognize a discrete
lesion.

7^V\s*^rs^\jKj<^>~^^

Etiology
The etiology of stroke in our patients
No patient had suffered
sufficient birth trauma to account for a
focal CNS injury and none had under¬
gone temporal artery catheterization.7
A definite cerebrovascular disorder
was present in ten patients. Four in¬
fants sustained a stroke following in¬

t^^Av/VfAAv>^^

was diverse.

trapartum or postpartum hypoxia-

Fig 3.—Patient 2. Electroencephalogram recorded on second day of life from infant with
infarction in distribution of right middle cerebral artery. Electrographic seizure is exquisitely
confined to right central region (calibration: 50 µ ", 2 s).

were

confirmed by recording simul¬

taneous electrographic seizures in six

patients. However, clinical observa¬

tion frequently underestimated the
true frequency or duration of seizures.
In five infants, one or more definite
electrographic seizures were recorded
that were not clinically detectable.
The majority of infants showed no
interictal lateralized clinical abnor¬
malities. Results of interictal clinical
neurologic examinations were normal
in two patients; nonlateralized abnor¬
malities (inactivity, generalized hypo¬
tonia, and lethargy) appeared in four
patients; and a subtle transient postic¬
tal hemiparesis appeared in three pa¬
tients. Only two infants had a mild
hemiparesis that persisted through
the neonatal period.
EEG

Electroencephalography revealed

clear evidence of a localized functional
CNS abnormality and correctly sug-

gested the presence and location of a

focal structural lesion in ten of 11 pa¬
tients. The electrographic abnormali¬
ties that most consistently correlated
with an underlying structural lesion
included persistent, localized voltage
reduction or attenuation (four cases),
prominent focal slowing and sharp
waves (four cases), and exquisitely
focal or lateralized seizures (five cases)
(Fig 3). There was excellent agree¬
ment between the site of origin of
electrogaphic seizures and the location
of stroke on CT scan.

Cranial Imaging
All of the initial CT scans obtained
one to five days following the onset of
neurologic signs revealed a localized
infarction. The CT appearance of all
the lesions was consistent with stroke
but none was verified neuropathologically. One was confirmed angiographically. Persistent localized infarction
was noted in all seven infants who

ischemia. Two infants were polycythemic at birth and hyperviscosity
was documented in one. Acute, severe,
prolonged hypertension arising from
renal compression and insufficiency
was the presumed etiology in one in¬
fant. Suspected or definite emboli
were responsible for focal CNS inju¬
ries in three patients. One infant had
two separate frontal infarctions and a
left atrial mass on echocardiography
compatible with myxoma or a mural
thrombus. The second infant had angiographically documented cerebral
emboli of an unknown source that may
have arisen in the venous system and
entered the cerebral circulation
through the foramen ovale, which is
patent until birth. The third infant was
born with a massive infarction of the
left cerebral hemisphere and ischemie
necrosis of the right arm due to subclavian artery occlusion proved by an

arteriogram. Although two separate
emboli were strongly suspected as the
cause, independent thrombosis of the
subclavian and carotid arteries re¬
mains a possible explanation.
Medical Management

Initial therapy was directed to gen¬
eral medical support and the aggres-

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sive administration of anticonvulsants
to control recurrent seizures. General
medical treatment included temporary
mechanical ventilation in five patients,
correction of coexisting metabolic ab¬
normalities in four patients, and sys¬
temic conditions (polycythemia and
hypertension) in three patients. None
of the infants with presumed cerebral
emboli were anticoagulated to avoid
precipitating a hemorrhagic infarc¬
tion. Serial EEGs were recorded from
the five infants in whom electro¬
graphic seizures were inconsistently
accompanied by clinical seizures.
Combinations of phénobarbital, phen¬
ytoin, and diazepam were adminis¬
tered aggressively until all clinical and
electrographic seizures were con¬
trolled. Anticonvulsants were discon¬
tinued at 3 to 6 months of age without
recurrence of seizures in nine patients.

Neurologic Outcome
The short-term neurologic outcome
of these patients was mixed. Seven

infants have been followed up for one

year or more. Five appeared entirely

well and exhibited normal develop¬
ment, neurologic examination results,
and EEGs. The hypertensive infant
who experienced prolonged coma and

status epilepticus (Table, patient 8)
subsequently microcephalic and
developmental^ delayed but not hemiparetic. Only one infant (Table, pa¬
was

tient 3) had a persistent hemiparesis.
COMMENT

The clinical syndrome of neonatal
stroke has been delineated in 11 infants
evaluated during a two-year period.
Stroke is relatively common in the
term neonate but difficult to recognize
by clinical examination alone. The ma¬
jority of infants presented with a cere¬
brovascular disorder heralded by re¬
petitive, persistently unifocal motor
seizures and clear EEG evidence of a
focal or lateralized functional abnor¬
mality. Although focal seizures may
follow diffuse encephalopathies, such
as asphyxia or metabolic abnormali¬
ties,8"10 the persistence of seizures
after metabolic correction and the
close agreement between the site of
origin of electrographic seizures and
the CT scan location of the lesions
indicate that the strokes caused the

focal seizures. In contrast to the high
incidence of unifocal seizures in this
group (eight [73%] of 11 patients), a
significantly lower incidence (two [8%]
of 24 patients) ( 2 12.33 with 1 df;
P<.01) of repetitive unifocal EEG sei¬
zures was recorded during the same
time period in 24 other full-term neo¬
nates with strictly global encephalopathies.
The focal or lateralized EEG abnor¬
malities observed in these infants are
etiologically nonspecific and are not
pathognomonic for stroke. However,
their presence emphasizes the value of
neonatal EEG in signaling the pres¬
ence of focal parenchymal injuries as
has been recently described by Scher
et al.u
Despite the high incidence of
unifocal motor seizures and localized
EEG abnormalities, the interictal
clinical neurologic and cranial ultra¬
sound examinations were frequently
insensitive to stroke. These observa¬
tions are in general agreement with
previous reports of stroke in neo¬
nates.1"4 Barmada et al3 reported a
5.4% incidence of cerebral infarctions
of arterial origin determined by post¬
mortem examinations of 592 infants
during a four-year period. No later¬
alized clinical abnormality had been
appreciated in any patient but 17%
suffered neonatal seizures. Mannino
and Trauner1 described five neonates
with strokes diagnosed by CT scan.
Four infants had normal cranial ultra¬
sound examination findings. Four also
had focal seizures but none displayed
lateralized clinical abnormalities.
However, Hill et al2 and Wilson-Davis
et al4 reported ultrasound stroke de¬
tection in a total of seven patients of
whom six experienced seizures. Only
three patients displayed lateralized
clinical signs.
The etiologies of stroke were heterogenous, but it is apparent that a vari¬
ety of generalized cerebrovascular dis¬
orders can cause localized cerebral
infarction in the neonate. Although
diffuse cerebral injury usually follows
global asphyxia, focal injury may also
result.12 A possible mechanism for this
has been suggested by Voorhies et al13
who demonstrated cerebral artery oc¬
clusion by digital intravenous an¬
giography in two of six severely as=

phyxiated neonates. Similarly, stroke,
neonatal seizures, and developmental
delay may follow the diffuse encepha¬
lopathy of polycythemia and hyperviscosity.14"16 The pathophysiology of
encephalopathy in the hypertensive
neonate is unknown but the neurologic
signs include coma, hemiparesis, and
seizures.17
Medical treatment of neonatal
stroke was conservative and included
careful management of cardiopulmo¬
nary status and the correction of con¬
current metabolic or systemic abnor¬
malities. The treatment of seizures
was

vigorously pursued. Although

these infants' seizures were the result
of their stroke, it remains possible that
the seizures were not innocent se¬
quelae but were partially responsible
for the extent or severity of the focal

parenchymal injury. Experimentally

induced focal seizures in newborn
monkeys elicit a sharp increase of cere¬
bral glucose utilization in several ipsilateral cortical and subcortical struc¬
tures.18 Electroencephalographic sei¬
zures in the human newborn are
virtually always focal or multifocal in
onset.19 Ten of our patients experi¬
enced repeated focal seizures and
probably had a local increase in the
cerebral metabolic rate. An NMR
spectroscopy examination in one pa¬
tient during recurrent seizures arising
from the left temporal-central-oc¬
cipital regions showed a virtual deple¬
tion of regional high-energy metabo¬
lites that persisted until the seizures
were stopped with anticonvulsants.
The ischemie nature of these focal cer¬
ebral injuries may limit the regional
availability of glucose and other meta¬
bolic substrates. The resulting un¬
coupling of cerebral blood flow and
metabolism could extend a limited ini¬
tial injury to cause more severe or
extensive localized infarction. The
therapeutic implication of these obser¬
vations is the aggressive use of anti¬
convulsants to promptly and com¬
pletely terminate seizures.
Although we are encouraged that
many affected infants are neuro¬
logically and developmentally normal
on short-term follow-up, the long-term
effects of stroke on language, cog¬
nitive, social, and fine motor develop¬
ment are unknown.

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In Other AMA Journals
JAMA
Motor Vehicle Childhood Injuries Caused by Noncrash Falls and Ejections
P. F. Agran, MD, MPH; D. E. Dunkle, PhD; D. G. Winn, RN, MPH (JAMA 1985;253:
2530-2533)
Current and Future Directions for Hospital and Physician Reimbursement
R. G. Petersdorf, MD (JAMA 1985;253:2543-2548)
SI Units for Clinical Laboratory Data
Council on Scientific Affairs (JAMA 1985;253:2253-2254)
AMA's 'Medicine Today' TV Program
L. D. Grouse, MD, PhD, T. Rockwell, MD (JAMA 1985;253:2558-2559)

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