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Child's Nerv Syst (1986) 2:195-199

© Springer-Verlag 1986

Cerebral infarction in term neonates: diagnosis by cerebral ultrasound
H. B o d e *, H . M . S t r a l 3 b u r g , W . P r i n g s h e i m , a n d W . K i ~ n z e r
Universit~ts-Kinderklinik, Mathildenstrasse 1, D-7800 Freiburg i. Br., Federal Republic of Gernaany

Abstract. Cranial ultrasound (US) through the n e w b o r n ' s
open fontanelle can diagnose not only intracerebral hemorrhages but also diffuse a n d localized hypoxic-ischemic
encephalopathies. Sonographically, it was possible to distinguish between different courses o f cerebral ischemia in
seven neonates: (1) ischemic infarction, usually in the area
o f the m i d d l e cerebral artery; (2) borderline infarction; (3)
transient ischemia. The patients showed lateralized seizures during the first days o f life with a corresponding
focus in the electroencephalogram (EEG). C o m p u t e d tom o g r a p h y showed areas o f partially r e d u c e d density corresponding t o the regions o f increased echogenicity in
ultrasound. The course was various; prognosis was good
except in one patient. Etiologically, embolism, thromboses
or h y p o x e m i a were responsible for cerebral infarction. In
some cases secondary bleeding ensued. The prognostic
value o f cerebral lesions was d e p e n d e n t on the involved
area, gestational age, and any concurrent hypoxic cerebral
damage.

Key words: Neonates -

Infarction e n c e p h a l o p a t h y - Ultrasound.

Hypoxic-ischemic

In the last few years intracranial bleeding o f the newborn,
especially o f the premature, has been o f increasing interest. This is particularly due to the new techniques o f
cranial C T a n d cerebral u l t r a s o n o g r a p h y (US). Only lately
has the possibility o f diagnosing hypoxic-ischemic changes
o f the n e w b o r n ' s brain been r e p o r t e d [6, 9, 14, 15, 20].
Generalized and localized lesions should be distinguished. In the term newborn, the latter Present as
ischemic infarction, usually in the area of the m i d d l e
cerebral artery, often with a typical clinical course, a n d
parasagittal borderline infarction [6, 10]. Periventricular
leucomalacia is the typical feature o f the p r e m a t u r e [5, 7].
Clinical course a n d prognosis in the two groups seem to be
different. This p a p e r does n o t deal with the latter.

* To whom offprint requests should be addressed

Materials and methods
We used two mechanical real-time sector scanners (ATL Mark 5
and ATL Mark 100) with a 5 MHz tansducer for the examination
of the newborn via the open fontanelle. Sedation was not needed.
Pictures were taken in different coronal and in the sagittal, and
different parasagittal planes. CT was done by a General Electric
8800 without contrast medium. EEGs were recorded with an 8channel EEG machine (Siemens mingograf 10). Electrode placement was according to the international 10-20 system.

Case reports
Patient 1

This boy was born on 23 August 1984 by normal vaginal delivery
in week 39 and weighed at birth 3,450 g. Apgar scores were 9-10-10
after 1-5-10 min. At 30 h after birth he had a tonic seizure and
showed opisthotonus. Serum electrolytes, blood sugar, pH status,
screening for amino acids and organic aciduria and serology for
perinatal infections were normal. Cranial US on day 2 demonstrated increased echogenicity of the right precental subcortical
area with finger-shaped reflexions laterally (Fig. 1). There were no
differences in vascular pulsations between the sides. The EEG on
day 11 demonstrated a right precentrotemporal epileptic focus.
The CT on day 14 revealed a right frontal hypodense area, no
necrosis, and no bleeding (Fig. 1). Under treatment with phenobarbitone no seizures occurred after day 4. At 5 weeks, the right
ventricle was larger than the left one; at 3 months small cystic
areas of necrosis were seen in US (like patient 2, Fig. 2). At 8
months the child showed slightly asymmetric movements (better
on the left side) with an otherwise normal development.
Patient 2

Jhis boy was born on 9 January 1984 by emergency caesarian
section in week 32 and weighed 1,940 g. The mother had toxemia
of pregnancy. Apgar scores were 4-10-10 after 1-5-10 rain. At the age
of 5 weeks the boy developed severe hypernatremic toxicosis with
epileptic seizures. CT showed diffuse frontal areas of low density
with additional diminished density in the right precentral area.
The EEG revealed epileptic activity in the same area. Cranial US
demonstrated a wedge-shaped area of increased echoes with the
apex at the foramen of Monro and the base near the left cortex. A
small cystic area of necrosis developed within 2 months, which
gained connection to the slightly enlarged ventricles after another
2 months (Fig. 2). No more seizures were seen under treatment
with phenobarbitone. At 6 months the child showed slight coordination problems.

196

Fig. 1. Patient 1. Ultrasound on day 2
(left): increased echogenicity of the
fight precentral area. Computerized
tomogram on day 14 (right): right
frontal hypodense area

Patient 3
This boy was born on 23 April 1984 and weighed 2,460 g. He was
delivered by caesarean section in week 38 because of severe
variable cardiac decelerations due to premature separation of the
placenta. Apgar scores were 4-6-9 after 1-5-10rain. On day 2
right-sided seizures occurred. The EEG showed an epileptic focus
in the left temporoparietal area. Cranial US demonstrated a leftsided horseshoe-shaped area of decreased echoes. The echoes
increased at its border during the next 2 days; a porencephalic
defect developed within 3 weeks. CT on day 4 had revealed a
flesh hematoma in the same area (Fig. 3.) The EEG showed a
corresponding epileptic focus. No more seizures occurred under
phenobarbitone. At 4 months the child showed moderate rightsided muscular hypertonia. The porencephalic defect persisted.
The histology of the placenta revealed an intervillous thrombus
and older infarction (Institute of Pathology, University of Freiburg,
no. 8590/1984).

features. CT on day 10 demonstrated diffuse areas of low density
in the subcortical area of both hemispheres. The child appeared
clinically normal at 3.3 years apart from speech retardation.

Patient 6
This boy weighed 2,600 g and was born at term on 6 May 1980
after a normal pregnancy. During labor, variable cardiac decelerations due to the umbilical cord encircling the neck were
recorded. Apgar scores were 8-10-10 after 1-5-10 rain. On day 3
right-sided tonic-clonic seizures appeared. Serum electrolytes,
blood sugar, pH status, screening for amino acids and organic
aciduria and serology for perinatal infections were normal. The
EEG on day 6 showed an epileptic focus in the left temporoparietal area. CT examination on days 6 and 15 revealed diffuse,
mainly frontocerebral edema. US on day 13 revealed increased
echoes in the left lateral fissure of Sylvius, which were no longer
visible 10 days later. The child was clinically normal at 3 and 6
months as was his EEG.

Patient 4
This girl was born on 20 May 1980 at term to a mother with toxemia
of pregnancy, the baby weighed 3,440 g. Uncomplicated delivery
and Apgar scores of 9-10-10 after 1-5-10 min were noted. Serum
electrolytes, blood sugar, pH status, screening for amino acids and
organic aciduria and serology for perinatal infections were normal. Within 24 h she developed right-sided tonic-clonic seizures
with a corresponding epileptic focus in the left precentral area in
the EEG. By US an increased echogenicity in the left central
subcortical area was detected. CT was negative. Fourteen days
later CT showed a hypodense area in the left temporopolar
region. Clinical findings and US were normal after another
2 weeks. At 1 year the child was still normal.

Patient 7
This baby was born on 31 December 1982, weighed 1,740 g, and
was small for the date of birth. Caesarean section was undertaken
because of placental insufficiency in week 37. Apgar scores were
2-7-10 after 1-5-10 min. Mechanical ventilation was necessary for
3 days because of the severe respiratory distress syndrome. On
day 3 generalized seizures were seen. US indicated generalized
cerebral edema; 3 days later there were zones of high echodensity
frontobasally, precentrotemporally, and in the areas of the lateral
fissures (Fig. 4). Three weeks later porencephalic defects were
seen in these areas, which could no longer be detected 8 months
later. This child developed cerebral palsy and epilepsy.

Patient 5

Discussion
This girl was born on 26 May 1981 at term after a normal
pregnancy and delivery; she weighed 3,120 g. Apgar scores were
9-10-10 after 1-5-10 rain. On day 5 right-sided seizures appeared.
Serum electrolytes, blood sugar, pH status, screening for amino
acids and organic aciduria and serology for perinatal infections
were normal. US on day 7 revealed increased echoes lateral to
both ventricles predominantly left-sided and reaching the cortex.
The EEG under phenobarbitone on day 9 showed no pathologic

I n a d d i t i o n to i n t r a c r a n i a l h e m o r r h a g e , h y p o x i c - i s c h e m i c
i n j u r y m a y cause b r a i n d a m a g e in the p e r i n a t a l p e r i o d [1,
8]. G e n e r a l i z e d a n d localized c h a n g e s can be distinguished. I n t e r m n e o n a t e transitory i s c h e m i a a n d c o m plete cerebral infarction, u s u a l l y in the r e g i o n s u p p l i e d
b y the m i d d l e cerebral arteries [6, 10], a n d b o r d e r l i n e

197

Fig. 2. Patient 2. Ultrasound at the
age of 5 weeks: left wedge-shaped
area of increased echos with the apex
at the foramen of Monro and the base
near the left cortex. Three months:
small cystic area of necrosis; 5
months: asymmetry of the slightly enlarged ventricles (left to right)
Table 1. Causes of cerebral infarction in neonates
Hypoxemia
perinatal hypoxia
severe anemia
failure of oxygenation (e.g., respiratory distress syndrome,
persistent fetal circulation)
Ischemia
postintraventricular hemorrhage
thrombosis
traumatic vascular damage
polycythemia °
stasis/shock
meningitis/encephalitis a
tumors and malformations
consumption coagulopathy
hypernatremic toxicosis
embofization
placental tissue/vessel thrombus
twin-to-twin transfusion syndrome
patent ductus arteriosus and foramen ovale
congenital heart disease
Arterial hypotonia
Venous circulation more commonly affected

Fig. 3. Patient 3. Ultrasound: left sided horseshoe-shaped area of

decreased echos (day 2) with increasing echos at its border (day 4).
Development of a porencephalic defect (day 20). Computed tomography (day 4): fresh hematoma in the same area

infarction [20] can be differentiated. The typical pattern in
the premature infant is periventricular leucomalacia [5, 7].
The latter condition will not be considered further in this
paper.
Pathologically, infarction is defined as a local necrosis
of part of an organ due to a localized disturbance o f

perfusion [41. Barmada [2] described an incidence of
cerebral infarcts following arterial occlusion of 17% in
term infants. Anomalies of circulation in perinatal conditions may explain the high incidence in autopsy material
[19]. Hemorrhagic infarcts were predominant with a peak
manifestation at 2 - 3 weeks after birth [11]. Histologically,
white spots with accumulation of macrophages containing
lipid in areas of gliosis were seen. Central liquefaction and
cyst formation and proliferation or congestion of small
vessels resulted soon in larger zones of hemorrhagic
infarction [3]. The localization o f infarcts in the term
neonate follows from the special vascular architecture of
its brain, which is quite different from that of the premature infant [18].
Causes o f hypoxia in newborn brains are (alone or in
combination) ischemia, hypoxemia and arterial hypotonia.
Table 1 shows the possible causes o f cerebral infarction in

198

Fig. 4. Patient 7. Ultrasound: zones of
high echodensity frontobasally, precentrotemporally and in the areas of
the lateral fissures

Table 2. Diagnosis, cause, outcome of cerebral infarction in our patients
Patient

Diagnosis

Cause

Outcome

1
2

Ischemic infarct of right m.c.a, a
lschemic infarct of left m.c.a. °

Not known
Hypernatremic
toxicosis

Slight asymmetry
Slight central coordination problems

3

Prenatal infarct of left m.c.a. ~
with secondary intraparenchymal
hemorrhage
Ischemic infarct of left m.c.a."
Transient ischemia of left and
right m.c.a?
Transient ischemia of left m.c.a?

Placental
embolus

Muscular hypertonus

Not known
Not known

Normal
Normal

Hypoxia

Normal

Borderline infarcts with secondary
intraparenchymal hemorrhage

Perinatal
hypoxia

Spastic cerebral palsy,
epilepsy

4
5
6
7

a

m.c.a., middle cerebral artery

neonates. They can, however, also be observed after a
totally uneventful perinatal period (patient 1). Infarcts of
intrauterine origin can be seen at birth. Embolization of a
placental thrombus through the ductus arteriosus or foramen ovale m a y be a major pathogenic mechanism
(patient 3). For causes of cerebral infarction in our patients see Table 2. Lesions m a y be unilateral (patients 1-4,
6), bilateral (patient 5), or at multiple sites (patient 7).
One should consider local cerebral ischemia if a
newborn shows symptoms like early apnea and especially
focal, nonmetabolic fits within the first days of life (patient
1-7). Hemiparesis was not seen in this age group.
Until lately, localized cerebral ischemia has rarely been
demonstrated in the newborn period. Cranial US and
CT especially have improved diagnostic facilities. The
particular value o f the latter shall not be discussed in
detail further. As a result of local ischemia, wedge-shaped
regions of increased echoes are found in the US of the
full-term neonate [9]. Their causes are not yet fully
understood [6]. Changed impedance due to extracel-

lular edema, incorporation of water or lipids into the
cytoplasm and the enlarged intracellular bodies, the development of necrosis, capillary congestion and extravasafion of blood corpuscles have been thought responsible
[15]. Sometimes the increased echos m a y even represent
sonographic artifacts.
The differentiation between infarction and vascular
congestion or hemorrhagic and nonhemorrhagi¢ infarction
by US alone is not always possible. Intracerebral bleeding
m a y be distinguished from hemorrhagic infarction by an
even greater increase of echogenicity, stronger expansive
tendency or localization. Porencephaly is more c o m m o n
and more coarse following hemorrhagic tissue lesions
(patient 3). Pure ischemia results more often in small cystic
lesions (patients 1 and 2). Small defects can disappear with
time (patient 7). Glial proliferation and calcification are
seen only after lesions of older children.
Postmortem correlation studies with the results of US
are still rare [5, 11, 13, 16]. We could not carry any out
either, because none of our patients died. Yet it is known

199
that confirmed (postmortem) cerebral edema can be diagnosed in US by the diffusely increased echogenity of the
brain parenchyma with ventricular compression and loss
of the interhemispheric fissure. One should expect analogous changes in localized ischemia.
So far, the final diagnosis can only be made by
repeated observations and the additional use of other
techniques such as EEG and CT, with and without
contrast medium. Further information may come from
cerebral scintigraphy, which should remain negative in the
1st week after infarction [12] as well as digital intravenous
angiography [19] and positron-emission tomography [18],
Doppler sonography [15], and magnetic resonance tomography. The different techniques may lead to different
results and variously localized alterations at synchronous
investigations and in the course of observation. Early
examinations are important for comparison; pathological
results beyond the 1st week are of greater prognostic
relevance than earlier ones. For example, the CT often
remains negative in the 1st week after cerebral infarction
or only shows generalized cerebral edema. A localized
reduction of density in the CT scan corresponding to the
region of increased echogenicity in US is detected only
later [9]. This supports the differential diagnosis between
hemorrhagic and ischemic infarction. The EEG frequently
shows epileptic discharges (patients 1-4, 6) corresponding to the localization of the infarct.
The prognosis of pure ischemia i n ' t h e newborn as
suggested by our experience and the literature [9] seems to
be good. So far, therapeutic considerations have not been
forthcoming. Undoubtedly, prophylaxis is important in
elimination of risk factors [20]. Unfortunately, follow-up
studies of larger groups are still awaited. Etiologically
unexplained mild hemiparesis, focal fits, porencephalic
defects, focal atrophies, and unilateral ventricular asymmetry may be the sequelae of infarction in the neonatal
period [9].
.
:;~
Finally, cerebral ischemia and intracran!~l: ~emorrhage
must not be considered as isolated entities. ~In the US of
some patients, we detected ischemic lesions as well as
hemorrhages of various extent. Using Doppler sonography, we saw decreased blood flow in the hemisphere
ipsilateral to the bleeding. This fact was already known
from positron-emission tomography [18]. Cerebral hemorrhage may even be a marker for underlying generalized or
localized hypoxia. Transtional stages are possible; their
extent is variable as can be seen in the transient ischemias
of patients 5 and 6.
The prognostic value of a single result of only one
method is limited. Thus, the prognosis of a sonographically
detected cerebral hemorrhage very much depends on the
simultaneous hypoxic-ischemic injury, which can only be
estimated by considering all available data and taking into
account the clinical course, the case history, and the result
of further diagnostic procedures.

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