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Cerebral infarcts with arterial occlusion in neonates.

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Cerebral Infarcts with
Arterial Occlusion in Neonates
M. A. Barmada, MD, J. Moossy, MD, and R. M. Shuman, MD
Among 592 infants examined at autopsy during a four-year period, 32 (5.4%)had cerebral infarcts. Excluded were
cases of traumatic hemorrhages and softening, periventricular leukomalacia, venous lesions, and any mass, including encephaloceles, with arterial distortion and infarction. Histological abnormalities were similar to those of
infarcts in adults. Relatively advanced histopathological changes in some infants living only a few hours indicated
that some infarctions may have occurred in utero. The most common cause of arterial occlusion was embolization,
with sepsis and disseminated intravascular coagulation playing a major role. The brains of term neonates were more
frequently involved than those of premature infants. Multiple small infarcts occurred more often in premature
infants. In most cases autonomic dysfunction with prolonged apnea, episodic seizures, and metabolic acidosis were
the major associated clinical features, rather than focal neurological deficits. Similar cerebral infarcts in infants who
survive with less severe systemic complications may lead to porencephaly, hemiplegia, mental and motor retardation, and recurrent seizures.
Barmada MA, Moossy J, Shuman RM: Cerebral infarcts with arterial occlusion in neonates.
Ann Neurol 6:495-502, 1979
The recent advent of neonatal intensive care units has
created a growing interest in the neurological features, prognosis, and rehabilitation of infants surviving various perinatal lesions including cerebrovascular accidents. The recognition that cerebral infarction
occurs in infancy and childhood is not new [6, 371.
Intracranial venous thrombosis has received the
greatest emphasis as the cause of these lesions [3, 16,
371. There are scattered reports of occlusion of major
cerebral arteries with large cerebral infarcts [ 8 , 9 , 11,
22, 30, 321. Small to medium-sized infarcts of arterial
origin in the newborn brain are often overlooked o r
misinterpreted as traumatic lesions if these infarcts
are hemorrhagic [ 191. More detailed information regarding the histopathology, topography, pathogene.
sis, and clinical features of infarcts of arterial origin in
the neonatal period is therefore desirable.
Materials and Methods
We confined our study of cerebral infarcts to those of the
recent past in neonates without cerebral malformations and
to those infants dying and autopsied in the neonatal period.
The neonatal period has been officially defined as the first
28 days of life [2]. Hemorrhages and softening due to
trauma, venous lesions, and any intracranial mass or tumor
associated with arterial distortion and infarction, including
encephaloceles, were excluded. Cases of periventricular
infarcts (leukomalacia) were excluded if the patient had no
associated cortical infarction. Hydranencephaly, porenFrom the Department of Pathology (Neuropathology), University
of Pittsburgh Medical Center, Pittsburgh, PA.
Accepted for publication May 6, 1979.
cephaly, schizencephaly, and multicystic encephalopathy
(polycystic brain) were excluded.
Brains removed at autopsy were fixed by immersion in a
10% solution of buffered formalin. Many of the premature
brains were perfused in situ with a solution of 20% buffered formalin before removal from the cranium. Arteries
at the base of the brain and within the sylvian fissures were
carefully examined for thrombi. Gestational age was determined from the expected date of delivery by menstrual
history, clinical examination of the infant, and maturation
of the gyral pattern of the brain [ 7 , 121. The cerebral hemispheres were sectioned in the coronal plane, the brainstems
in the horizontal plane, and the cerebellum in the sagittal
plane. All suspected and evident lesions were sampled
for microscopic examination, embedded in paraffin, sectioned, and stained with hematoxylin and eosin. In addition, Nissl, myelin, phosphotungstic acid-hematoxylin,
Bielschowsky’ssilver, and Masson’s trichrome stains were
used in some cases. The clinical charts of each baby and
mother were reviewed for pertinent clinical information.
The diagnosis of disseminated intravascular coagulation
(DIC) was accepted when the platelet count was 80,000 or
less, prothrombin time and partial thromboplastin time
were elevated, and fibrin-platelet thrombi were noted in at
least two organs at autopsy. The diagnosis of sepsis was
accepted only when the patient had evidence of bacterial
growth in antemortem blood culture.
There were 592 autopsied neonates in the four-year
period surveyed. Thirty-two patients had cerebral
Address reprint requests to Dr Barmada, Department of Pathology, Magee-Women’s Hospital, Forbes & Halket Sts, Pittsburgh,
PA 15213.
0364-5134/79/120495-08$01.25 @ 1979 by M. A. Barmada 495
infarcts in the arterial distribution, a prevalence of
5.4%; 29 had material suitable for detailed clinicopathological investigation.
Demographic Findings
The neonates with cerebral infarction ranged in gestational age from 29 to 40 weeks, with 5 babies
(17%)from 29 to 32 weeks, 10 (34%) from 33 to 37
weeks, and 14 (48%)from 38 to 40 weeks. This is in
contrast to the distribution of gestational ages in the
autopsy population derived from the neonatal intensive care units of Magee-Women’s Hospital and
Children’s Hospital: neonates of 28 weeks’ gestation
or less made up 48%, 29 to 32 weeks’ gestation 2095,
33 to 37 weeks’ gestation 16%, and term infants only
16% of the autopsy population. The babies with
neonatal cerebral infarction were predominantly
from the older gestational ages (p = 0.001, Table 1).
The prevalence of cerebral infarcts was the same in
white versus black neonates. The male to female sex
ratio in the neonatal autopsy population at MageeWomen’s Hospital was 59/41. The prevalence of cerebral infarcts in males exceeded that in females
6.10% to 4.39%.
Clinical Features
Clinical manifestations in these infants were different
from those in older children or adults with cerebral
infarcts, and focal neurological deficits such as
hemiplegia were not reported (Table 2). Generalized
hypotonia was the most frequent clinical manifestation. Most of the infants became suddenly lethargic
and unresponsive except to deep pain. Spontaneous
movements and even primitive reflexes were frequently suppressed. Autonomic instability was prominent. All 29 infants suffered at least one of the
following signs: bradycardia, apnea, cyanosis, or
hypotension. A 2 1% incidence of hypoglycemia was
similar to that seen in the general high-risk infant
population. Even though all infants were cared for by
experienced neonatologists, the frequency of convulsions is probably underestimated since seizures in the
neonate, particularly premature infants, may manifest
themselves as sudden episodes of apnea, bradycardia,
hypotonia, and/or sudden fleeting movements of the
eyes, brief tonic episodes, and other subtle clinical
manifestations not usually recognized as convulsive.
Electroencephalograms (done in only 3 infants) were
nonspecific; two were compatible with generalized
seizure activity, and the third showed focal spike activity, a pattern often found in normal premature infants of 30 to 34 weeks’ gestation. Three of 5 patients
with convulsions had associated intraventricular
Most of the neonates in our study had died rapidly
following the occurrence of their cerebrovascular in-
Table 1. Distribution of Gestational Ages
in the Entire Neonatal Autopsy Population
versus the Population with Cerebral Infarcts
No. of Patients
Age (wk)
No Cerebral
Table 2. Clinical Features in 29 Neonates Who Had
Cerebral Infarcts with Arterial Occlusion at Autopsy“
Movement only with pain
Weak bilateral grasp reflex
Absent Moro reflex
No. of
aMost patients had two or more clinical features.
sult (Fig 1 ) . By five days after birth 50% of the patients were dead; at 10 days more than 75% had died.
One baby survived 5 5 days after a clinically defined
cerebrovascular episode that had occurred on the
second day of life; the child finally died with recurrent apnea.
Neonatal Complications
Eighteen neonates had DIC, associated in most with
sepsis or respiratory distress syndrome (RDS) or secondary to surgery (Table 3). Thirteen had a prolonged
episode of cardiorespiratory arrest or sudden prolonged hypotension. Metabolic acidosis was a frequent finding in all infants and may have been an
important contributory factor. In contrast to the case
in older children, congenital heart disease (CHD)
was not an important etiological factor of cerebral
infarction in neonates. Periventricular infarcts (leukomalacia) were noted in 6 patients who also had
cortical infarcts. Intraventricular and germinal matrix
hemorrhages were present in only 5 patients. Multiple associated neonatal complications were found in
many patients and may have contributed to cerebral
arterial occlusions. The association of DIC and sepsis
496 Annals of Neurology Vol 6 N o 6 December 1979
1 ;1 ' '
1 5I . .
Fig 1. Survival curve of 29 neonates who had cerebral infarcts
with arterial occlusion at autopsy.
with multiple small infarcrs and that of RDS or C H D
with single large infarcts is notable (see Table 3).
Maternal Complications
Maternal complications were few and did not seem to
play a major causative role in neonatal cerebral infarction except for a few cases in which infarcts may
have occurred a few days before delivery or during a
prolonged and difficult labor. Cesarean-section delivery was necessary for 6 infants (20% of the infarct
population). A random sampling of the well-baby
clinic at Magee-Women's Hospital showed a 10%
incidence of cesarean sections. Premature rupture of
membranes occurred in 4 mothers, toxemia in 2, diabetes mellitus in 2 , and placenta previa in l . Amniocentesis was performed in 2 cases. The incidence
of these maternal complications was similar to that in
our control population of the well-baby clinic.
Neuropathological Findings
Large infarcts predominated slightly in full-term infants. Premature infants more often had multiple
small infarcts. Of the 15 premature infants ranging in
gestational age from 29 to 37 weeks, 5 had large,
unifocal infarcts and 10 had small to medium-sized
infarcts, often adjacent to a small thrombosed artery
or arteriole. Of the term infants (14 cases, gestational
age 38 to 40 weeks), 8 had large, unifocal cerebral
infarcts while 6 had multiple small infarcts.
The major arterial distribution involved was the
left middle cerebral artery (LMCA), which was the
site of infarction in 9 cases (Table 4). The right middle cerebral artery (RMCA) was affected in 5 cases.
Only 1 case of occlusion of the basilar artery occurred. Two premature infants had multiple infarcts
located exclusively in the territories of the middle
cerebral arteries, and these 2 cases are tabulated
among those with a major arterial distribution. Arterial thrombosis was found in slightly more than half
of the cases. The other 14 neonates with infarcts had
multiple small arterial lesions, some without occlusion and some with fibrin-platelet thrombi.
The gross and microscopic features of the infarcts
were similar to such lesions in adults. Microscopically, there was severe disorganization or complete
disruption of the neuronal architecture of the cortex.
Pyknotic eosinophilic neurons, foamy macrophages,
and a few astrocytes, depending on the age of the
infarct, made up the cellular constituents, accompanied by varying degrees of capillary prominence
and neovascularization. The full thickness of the
cortex and subcortical white matter was usually involved. Hemorrhage into originally ischemic infarcts
was frequent, unlike the situation in adults, in whom
most ischemic infarcts remain ischemic or consist of
patchy mixtures of ischemic and hemorrhagic zones.
Gross and microscopic features of the cerebral infarcts correlated closely with the clinical histories.
Figure 2 shows a coronal section from the brain of a
full-term infant (Table 3, Case 28) who lived only
two days after developing respiratory distress secondary to meconium aspiration. A thrombus was
found in the LMCA. In another case (Table 3, Case
12), a boy of 36 weeks' gestation with a large hemorrhagic infarct in the brain, a thrombus was present in
the RMCA. This infant was born with C H D and
Barmada et al: Cerebral Infarcts in Neonates 497
Table 3. Neonatal Clinical Complications i n 29 Neonates Who Had Cerebral Infarcts with Arterial Occlusion
Case No.,
GA (wk),
and Sex
1. 29, M
2. 30, F
3. 32, F
4. 32, M
5. 32, M
6. 33, M
7 . 33, M
8. 33, M
9. 34, M
10. 34, M
11. 35, F
12. 36, M
13. 36, M
14. 36, M
15. 36, F
16. 38, F
17. 38, M
18. 38, M
19. 38, F
20. 38, M
21. 38, F
22. 39, M
23. 40, F
24. 40, F
25. 40, F
26. 4 0 , F
27. 40, M
28. 40, M
29. 40, M
GA = gestational age; DIC = disseminated intravascular coagulation; RDS = respiratory distress syndrome, including hyaline membrane
disease and meconium aspiration; CRA = cardiorespiratory arrest; JBP = sudden drop in blood pressure; C H D = congenital heart disease;
PVL = periventricular leukomalacia; IVH = intraventricular hemorrhage; RMCA = right middle cerebral artery; LMCA = left middle
cerebral artery; RMCA" = many in RMCA territory; LMCA" = many in LMCA territory.
Table 4. Major Arterial Distribution
of Cerebral Infarcts Associated with
Arterial Occlusion in 20 Neonates
No thrombus
"In 14 cases, multiple small arteries were involved.
LMCA = left middle cerebral artery; RMCA = right middle cerebra1 artery; BA = basilar artery.
Annals of Neurology Vol 6 No 6 December 1979
F i g 2. Coronalsection from the brain of a full-term infant
with thrombosis of the left middle cerebral artery and a large
ischemic infarct. The baby lived only two days after developing
respiratory distress secondary to meconium aspiration at birth.
anomalous pulmonary venous return, and lived only
one day. In other cases, multiple fibrin-platelet
thrombi were seen in the brain and other organs adjacent to multiple hemorrhagic infarcts, as illustrated
in the case of an infant of 33 weeks’ gestation (Table
3, Case 6). This child had erythroblastosis fetalis secondary to Rh incompatibility. The presence of macrophages and astrocytes around the lesion suggested
an infarct older than 22 hours, the postnatal survival
period. The last trimester of the pregnancy had been
closely followed, with repeated amniocenteses. Decreased fetal reactivity and a suspicious oxytocin
challenge test (OCT) were noted one week before
delivery. When the OCT was repeated a week later,
it was positive with late decelerations. The baby was
delivered by cesarean section.
A 32-week-gestation baby (Table 3, Case 3) with
C H D and severe coarctation of the aorta had a welldocumented episode of cardiorespiratory arrest, after
which he survived nine days. The infarct in this case
was chiefly in the cortex adjacent to a deep sulcus in
the superior parietal lobule, although the subcortical
white matter was affected too. The general autopsy
also revealed multiple thromboemboli in the lungs
and kidneys, a large thrombus filling iliac and renal
arteries, and a recent infarct of the right kidney.
Another infant (Table 3, Case 27), a full-term baby
receiving factor IX (Konyne) therapy for hemophilia
B, died with multiple arterial and venous occlusions
and recent infarcts of both kidneys and the brain. A
large thrombus was found extending from the aorta
into the iliac and renal arteries. Small arteries and
arterioles were thrombosed in multiple foci in the
“On the influence of abnormal parturition, difficult
labours, premature birth and asphyxia neonatorum,
on the mental and physical condition of the child,
especially in relation to deformities,” is the title of an
influential report presented by Little in 1861. This
study, published in 1862 [31], led to the well-known
eponym Little’s disease for the syndrome of infantile
spastic diplegia. Thereafter a confusing era began,
wherein many poorly defined intrauterine and
perinatal events, chiefly infectious and vascular disorders, were thought to injure the brain of the neonate. According to Bertrand and Bargeton [6],
Cotard in 1868 was the first to show the role of a
vascular factor in “cerebral atrophy.” In 1873 Parrot
[371 emphasized venous stasis and thrombosis as
causes of infarction in the neonatal brain, although he
was aware that intracranial arterial occlusion was important in some cases. In a review of 70 cases of
acquired infantile hemiplegia among more than
50,000 case histories from the Harriett Lane Home
in Baltimore, Ford and Schaffer [16] concluded that
infantile hemiplegias associated with acute infectious
diseases were due to vascular lesions. They reached
no final conclusions concerning the cause of hemiplegias that occur in apparently healthy children. Such
cases puzzled many authors. Gowers stated that fiveeighths of all infantile hemiplegias were apparently
primary [16]. A variety of arteriopathies have been
described with infantile cerebral infarction [6, 18,20,
341. Isolated case reports have mentioned the occurrence of cerebral infarcts with arterial thrombosis in
neonates, with some cases thought to be due to intrauterine placental infarcts with cerebral embolization [8, 91 and others to trauma at birth [14, 431.
Forty-eight cases of cerebrovascular occlusive disease in infants and children were evaluated by
Banker [31 in a review of 5 55 autopsies, a prevalence
rate of 8.7%. Arterial occlusion was present in 16
cases compared to 28 instances of venous occlusion.
Of her 16 examples of arterial occlusion, 3 occurred
in neonates among a total of 32 neonatal autopsies,
whereas only 1 of the 28 cases of venous occlusion
occurred in the neonatal period. Our four-year
population of 592 neonatal autopsies included 32
cases with infarcts in an arterial distribution and 14
cases of venous obstruction. Cerebral arterial disease
therefore appears to be more frequent in the
neonatal period than venous thrombosis. This may
be contrasted with a greater frequency of venous
thrombosis in older infants and small children [3,16].
The prevalence of cerebral infarcts of arterial origin in neonates is higher in our series than has previously been reported [3, 201. The higher prevalence
rate in our study may be due to the longer survival of
sick neonates cared for in neonatal intensive care
units, to unavoidable exposure to procedures such as
arterial catheterization, surgery, or massive antibiotic
treatment which predispose to thrombotic complications, and to improved postmortem diagnosis of
cerebral infarcts by perfusion of the brain before removal. Many recent reports document an improved prognosis for the premature infant cared for
in neonatal intensive care units, with a decreased incidence of cerebral palsy [171. However, the contradiction is only apparent. Cerebral infarcts with
arterial occlusion have often been overlooked as an
etiological factor in the clinical syndrome of cerebral
palsy [241.
The distribution of gestational age in our population with cerebral infarction in the neonatal period
differs statistically from that of the general perinatal
autopsy population. There appears to be an excess
(55%) of mature full-term infants in the neonatal
population with cerebral infarcts. A greater susceptibility to intravascular thrombosis in mature versus
premature neonates was demonstrated in a study of
Barmada et al: Cerebral Infarcts in Neonates
intravascular and cardiac thrombosis in the neonate
[ 151; patients with cardiac thrombosis were the
largest of the newborn infants. Depletion of
fibrinolysins in severe idiopathic respiratory distress
syndrome (IRDS) has been incriminated [231 as a
cause of hypercoagulability in premature infants with
hyaline membrane disease (HMD). Also, the low
levels of antithrombin I11 noted in infants with IRDS
might cause an increase in platelet adhesiveness because of greater amounts of thrombin [33].However,
the occurrence of H M D in mature neonates is unusual. Mature neonates have higher levels of factor
VIII [23] than do premature infants or older children. They also d o not suffer the same platelet dysfunction as premature infants [ 151. Therefore, increased levels of free fatty acids in severely hypoxic
infants may cause increased platelet aggregation.
Disseminated intravascular coagulation played a
major role in the pathogenesis of arterial occlusion in
our patients. DIC is frequent in the neonate [26] and
may reflect a nonspecific response to one or more
insults, including surgery and sepsis [lo, 2 3 , 391.
The diagnosis of neonatal DIC is difficult. Degradation products of fibrinogen or fibrin split products
(FSP) are frequently increased in DIC but are not
limited to that disorder in neonates. Hathaway et a1
[26] found no FSP in 5 of 8 cases of probable DIC,
while most infants with mild illness and no evidence
of DIC had FSP. The diagnosis of D I C in our study
was based on clinical evidence of a bleeding diathesis
[ 2 8 ]and the demonstration of fibrin-platelet thrombi
in two or more organs at autopsy.
In our study, arterial occlusion was due to DIC in 9
of 11 cases with sepsis. Arteritis with occlusion due
to acute leptomeningitis was present in the remaining
2 cases. All 9 patients who underwent surgery had
DIC. DIC was especially implicated in the pathogenesis of multiple, small, cerebral infarcts in which
necrotic brain surrounded blocked small arteries and
arterioles. Since other organs were invariably involved with lesions of DIC, a systemic disorder was
certainly present.
Thrombotic complications in neonates with umbilical vessel catheters may be arterial or venous, depending on the site of catheter placement [ 4 2 ] .Since
multiple factors such as the need for RDS monitoring
and the presence of acidosis, hyperviscosity, or
hypoxia often coexist and lead to the decision to insert a catheter, it is difficult to single out any one
overriding factor in the pathogenesis of cerebral infarcts [4, 131.
The pathogenetic role of many other factors in
these neonates was also difficult to evaluate. For
example, 2 infants with cerebral infarction had
meconium aspiration. Whether the aspiration led to
cerebral infarction because of subsequent hypox-
emia, acidosis, and hyperviscosity, o r whether it
was epiphenomena1 o r even secondary to the acute
cerebrovascular accident, was difficult to determine.
Another example was that of an infant whose mother
was subjected to amniocentesis one week prenatally;
the baby was found to have a cerebral infarct older by
histopathological criteria than his postnatal age.
Maternal factors, e.g., toxemia, placenta previa,
infection, or hemorrhage, did not seem to influence
the prevalence of perinatal cerebral infarcts. The incidence of these complications was the same as that
noted in the well-baby clinic. Although infants of
diabetic mothers reportedly develop intravascular
thrombosis more often [36, 411 than infants of nondiabetic mothers, this did not influence the number
of cerebral infarctions in our population. Cesarean
sections were more frequent ( 2 0 % ) in our population of cerebral infarcts than in the mothers of children in the well-baby clinic (lo%), but this may
reflect the fact that prenatal distress was more frequent in the population with perinatal infarcts. The
poorly defined etiological role of maternal complications was also noted by Goutieres et a1 [2 11 in a study
of 185 cases of infantile congenital hemiplegias.
The role of steroids in the formation of intravascular thrombi is also of speculative interest. The last
trimester of gestation is a period of high steroid
levels [ 3 8 ] . Since steroid hormones are known to
cause endothelial hyperplasia and to increase platelet
adhesiveness [4, 5 , 271, they might act by a mechanism similar to that producing endothelial proliferation and thrombosis in young women on birth control pills [27] or to the endothelial damage and
generalized thromboses in homocystinuria [251.
Whether exposure to maternal steroids in the
neonatal period is a pathogenetic factor in cerebral
infarcts in the neonate remains unknown.
The type of brain damage caused by intracranial
vascular occlusion is different in intrauterine life, at
various gestational ages, and in the neonatal period,
as compared to damage occurring in children and
adults [ 2 0 ] . These differences range from complete
anencephaly attributed to ischemia [ 4 0 ] , to hydranencephaly or porencephaly [32, 351. We excluded these disorders from our study even though
they have been attributed to arterial disease, by inference in human cases [ 3 2 ] and because of experimental manipulations in animals [351. Morphological
changes in the arteries in these cases may be absent
or otherwise obscured by the passage of time.
The different types of brain damage were described by Larroche [ 2 9 , 301 in 6 cases of cerebral
infarction due to thrombosis of the LMCA. Infarcts
early in fetal life produced focal cortical neuronal cell
loss and cytoarchitectonic abnormalities similar to
those seen in microgyria. Infarcts late in intrauterine
500 Annals of Neurology Vol 6 No 6 December 1979
life resembled those seen in adults, in that they were
cavitary in varying degrees with phagocytes, marginal
astrocytosis, and occasional mineralized nerve and
glial cells. Infarcts in the neonatal period were
characterized by severe cortical necrosis and hemorrhage in the cortex and subcortical white matter.
Friede [ 191 also stressed the hemorrhagic nature of
acute cerebral infarcts of arterial origin in neonates.
He reported 5 cases of small to medium-sized cerebral infarcts in newborns, 3 hemorrhagic and 2 ischemic. The rapid lysis of thrombi in neonates [ 2 3 ,
331 because of circulating fibrinolysins may be responsible for hemorrhage into cerebral infarcts, since
damaged capillary endothelium is thereby subjected
to renewed hydrostatic pressure. Rapid lysis of intravascular thrombi may also explain our inability to
detect arterial occlusion in some cases even though
the infarct may be localized within well-defined arterial territories.
The clinical picture associated with infarcts in the
neonatal period was chiefly that of generalized cardiovascular collapse with lethargy and hypotonia.
Focal neurological deficits were conspicuously absent, due in part to the rapid clinical course and in
part to the overwhelming systemic abnormalities.
The low frequency of seizures occurring in association with cerebral arterial thrombosis had already
been stressed by Aicardi et a1 [l] in a study of acute
hemiplegia in infancy and childhood. Most of the
neonates in our study died a few days after the cerebrovascular insult from associated or predisposing
systemic disorders and not primarily because of the
cerebral infarcts. If infants survive with cerebral infarcts such as we have described, they presumably go
on to develop porencephaly , hemiplegia, mental and
motor retardation, and recurrent seizures.
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Vol 6 No 6 December 1979
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infarcts, occlusion, neonate, cerebral, arterial
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