1990;85;737Pediatrics
Elke H. Roland, Olof Flodmark and Alan Hill
Thalamic Hemorrhage With Intraventricular Hemorrhage in the Full-Term Newborn
/>the World Wide Web at:
The online version of this article, along with updated information and services, is located on
ISSN: 0031-4005. Online ISSN: 1098-4275.
PrintIllinois, 60007. Copyright © 1990 by the American Academy of Pediatrics. All rights reserved.
by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village,
it has been published continuously since 1948. PEDIATRICS is owned, published, and trademarked
PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly publication,
at Viet Nam:AAP Sponsored on February 10, 2014pediatrics.aappublications.orgDownloaded from at Viet Nam:AAP Sponsored on February 10, 2014pediatrics.aappublications.orgDownloaded from
PEDIATRICS Vol. 85 No. 5 May 1990 737
Thalamic Hemorrhage With Intraventricular
Hemorrhage in the Full-Term Newborn
Elke H. Roland, MD; Olof Flodmark, MD, PhD; and Alan Hill, MD, PhD
From the Division of Neurology, Department of Pediatrics, and Department of Radiology,
University of British Columbia, British Columbia’s Children’s Hospital,
Vancouver, British Columbia, Canada
ABSTRACT. Intraventricular hemorrhage is an uncom-
mon problem in the full-term newborn. In a review of 19
full-term infants with intraventricular hemorrhage diag-
nosed on computed tomography prior to 1 month of age,
thalamic hemorrhage associated with the intraventricular
hemorrhage was documented in 12 infants. Thus, tha-
lamic hemorrhage appears to be the most common source
of intraventricular hemorrhage in this age group, partic-
ularly in infants who had uneventful birth histories and
in whom clinical abnormalities (signs of increased intra-
cranial pressure, seizures, altered level of consciousness)
developed after the first week of life. The majority of
these infants had predisposing factors for cerebral venous
infarction such as sepsis, cyanotic congenital heart dis-
ease, and coagulopathy. The clinical appearance and out-
come for infants with thalamic hemorrhage/intraventric-
ular hemorrhage were similar to those in infants with
intraventricular hemorrhage originating from other
sites, except for an increased incidence of cerebral palsy
in infants with thalamic hemorrhage/intraventricular
hemorrhage. Definitive diagnosis was made on the basis
of characteristic radiologic abnormalities. Pediatrics
1990;85:737-742; thakimic hemorrhage, intraventricular
hemorrhage, newborn, cerebral infarction.
Intraventricular hemorrhage occurs commonly in
the premature infant as a result of rupture of fragile
vessels in the subependymal germinal matrix. In
contrast, intraventricular hemorrhage occurs much
less frequently in the full-term newborn. Docu-
mented sources of hemorrhage in this age group are
more diverse and include residual germinal matrix,
choroid plexus, vascular malformation or tumor, as
well as extension of hemorrhagic cerebral infarc-
tion. Occasionally, intraventricular hemorrhage
may result from coagulopathy.”2
In a review of 19 full-term newborns with intra-
ventricular hemorrhage, we identified an unusually
high incidence of thalamic hemorrhage in associa-
tion with the intraventricular hemorrhage. In this
study, we describe the clinical appearance, associ-
ations, and radiologic features and sequelae at 18
months of age in this group of infants. In addition,
we provide a review of the literature on the uncom-
mon entity of thalamic hemorrhage/intraventricu-
lar hemorrhage in the full-term newborn.
METHODS
Study Population
The study population comprised all full-term
newborns (1 1 boys, 8 girls) admitted to British
Columbia’s Children’s Hospital between January
1980 and May 1987 in whom intraventricular hem-
orrhage was diagnosed by computed tomography
(CT) prior to 1 month of age. This hospital, the
only pediatric tertiary referral center for the prov-
ince of British Columbia, has approximately 39 900
full-term deliveries per year. Infants who had intra-
cerebral, subdural, subarachnoid, or posterior fossa
hemorrhage without accompanying intraventricu-
lar hemorrhage were excluded. We reviewed the
clinical and radiologic features as well as the out-
come of infants who had thalamic hemorrhage in
association with intraventricular hemorrhage.
Radiologic Investigations
Received for publication May 2, 1988; accepted Jun 2, 1989.
Reprint requests to (A.H.) Division ofNeurology, British Colum-
bia’s Children’s Hospital, 4480 Oak St, Vancouver, British Co-
lumbia, Canada V6H 3V4.
PEDIATRICS (ISSN 0031 4005). Copyright © 1990 by the
American Academy of Pediatrics.
CT scans of the head without contrast enhance-
ment were performed on all infants, often at the
referring hospital at the time of onset of clinical
abnormalities. Later, follow-up CT scans were per-
formed both with and without contrast enhance-
at Viet Nam:AAP Sponsored on February 10, 2014pediatrics.aappublications.orgDownloaded from
738 THALAMIC HEMORRHAGE AND NEWBORN
ment on all infants at least 3 weeks following the
original diagnosis of intraventricular hemorrhage
in an attempt to identify underlying cerebrovascu-
lar abnormalities. Scans were performed with a
General Electric 8800 CT/T scanner. Axial and
coronal sections of 5-mm thickness were viewed
using a window width of 60 Hounsfield units and a
window level of 30 Hounsfield units.
Cerebral ultrasonography was not performed rou-
tinely at the onset of clinical abnormalities, either
because of lack of easy availability of the technique
at the referring hospitals during the initial years of
the study or because it was considered redundant
following diagnosis by CT. Serial cranial ultrasound
scans were performed to document posthemor-
rhagic ventricular dilation. Cerebral angiography
was performed in three of the infants with thalamic
hemorrhage/intraventricular hemorrhage. Rapid
sequence, including late venous phase images, was
obtained using a magnification technique.
Neurologic Outcome
Neurologic examination was performed by a pe-
diatric neurologist on all infants at 18 months of
age. Developmental outcome was assessed accord-
ing to the Gesell Developmental Scale and was
classified as follows: (1) normal; (2) mild/moderate
delay-mild abnormalities of muscle tone that did
not interfere with ambulation; (3) severe delay-
developmental level of less than a 12-month age
level, ie, impaired ambulation often associated with
spastic quadriplegia, microcephaly, and seizures.
The incidence of neurologic sequelae in infants with
thalamic hemorrhage/intraventricular hemorrhage
was compared with that of infants with intraven-
tricular hemorrhage from other sources.
Statistical Analysis
The incidence of neurologic sequelae in infants
with thalamic hemorrhage/intraventricular hem-
orrhage as compared with those with intraventric-
ular hemorrhage from other sources was analyzed
statistically by means of the two-tailed version of
the Fisher exact test.
RESULTS
Radiologic Features
Review of the CT scans of the 19 full-term infants
with intraventricular hemorrhage demonstrated in-
creased tissue attenuation in the region of the thal-
amus, consistent with unilateral thalamic hemor-
rhage as the most probable source of intraventric-
ular hemorrhage in 12 infants (63%, Fig 1). The
presence of localized subependymal hemorrhage in
association with intraventricular hemorrhage sug-
gested residual germinal matrix as the source of
hemorrhage in three infants (16%). In 4 infants
(21%), no definite source of hemorrhage could be
identified and intraventricular hemorrhage was
presumed to originate most probably from choroid
plexus.
Decreased tissue attenuation suggestive of tha-
lamic infarction adjacent to the hemorrhage in the
thalamus was shown in the CT scans of three of
the infants with thalamic hemorrhage/intraventric-
ular hemorrhage performed during the acute phase
of illness (Fig 2). Furthermore, increased attenua-
tion in the region of the straight sinus (Fig 1) was
observed on noncontrast CT scans of two other
Fig 1. Noncontrast CT scan of brain of full-term new-
born with thalamic hemorrhage/intraventricular hemor-
rhage. Note increased attenuation in location of straight
sinus (arrow).
Fig 2. Noncontrast CT scan of brain of full-term new-
born with thalamic hemorrhage/intraventricular hemor-
rhage. Note decreased tissue attenuation (arrow) in thai-
amus adjacent to hemorrhage in thaiamus.
at Viet Nam:AAP Sponsored on February 10, 2014pediatrics.aappublications.orgDownloaded from
ARTICLES 739
patients with thalamic hemorrhage/intraventricu-
lar hemorrhage. In one patient, failure of opacifi-
cation of the ipsilateral internal cerebral vein
suggestive of venous occlusion was shown in cere-
bral angiography (Fig 3). In this patient, the vein
of Galen, inferior sagittal sinus, and straight sinus
appeared normal angiographically. No abnormal
attenuation in the straight sinus was shown in CT
scan. Angiographic results were normal in the two
other infants.
In all patients, follow-up contrast-enhanced CT
scans obtained at least 3 weeks after the initial
diagnosis of intraventricular hemorrhage did not
demonstrate unusual areas of enhancement sugges-
tive of vascular malformations. In addition, there
was normal filling of major cerebral venous sinuses
with contrast material.
Clinical Features
All infants with intraventricular hemorrhage had
sudden onset of dramatic neurologic abnormalities.
Prior to this presentation, 16 infants appeared nor-
mal. Of the 7 infants in whom intraventricular
hemorrhage developed before 2 days of age, 3 had
moderate hypoxic-ischemic encephalopathy. Clini-
cal features were nonspecific for the site of origin
of the intraventricular hemorrhage and included
one or more of the following: vomiting, seizures,
apnea, lethargy, irritability, bulging fontanel, and
Fig 3. Cerebral angiogram, venous phase, demonstrates
nonopacification of internal cerebral vein at time of
visualization of inferior sagittal sinus (arrow). These two
vascular structures are normally visualized simultane-
ously.
TABLE 1. Time of Onset of Clinical Abnormalities in
Full-Term Infants With Intraventricular Hemorrhage
Origin of No. of Infants
Intraventricular
Hemorrhage “Early Onset” “Late Onset”
<48 H 3-28 D
ofAge of Age
(n=7) (n=12)
Thalamus 2 10
Residual germinal matrix 3 0
Unknown (possibly choroid 2 2
plexus)
abnormal movements, eg, opisthotonic posturing or
jitteriness.
The ages at onset of clinical abnormalities of
patients in our series are listed in Table 1. The
. clinical and radiologic features of the 12 infants in
this series who had thalamic hemorrhage/intraven-
tricular hemorrhage as well as 8 additional infants
described previously in the literature are summa-
rized in Table 2. In the 7 infants in whom abnor-
malities occurred early, ie, prior to 48 hours of age,
hemorrhage originated from residual germinal ma-
trix in 3 infants, and most probably originated from
choroid plexus in 2 infants. Only 2 infants with
thalamic hemorrhage/intraventricular hemorrhage
(patients 7 and 9 in Table 2) had clinical abnor-
malities during the first 2 days of life. In 3 infants
in whom symptoms developed early, including 1
infant with thalamic hemorrhage/intraventricular
hemorrhage (patient 9), there was evidence sugges-
tive of acute birth asphyxia, eg, Apgar scores of less
than 5 at 5 minutes or need of positive pressure
ventilation for longer than 2 minutes following
delivery.
In 12 infants, the birth histories were uncompli-
cated and clinical abnormalities did not become
evident until later, between 3 and 28 days of age
(mean 10 days). Of the 12 infants with thalamic
hemorrhage/intraventricular hemorrhage, 10 were
in this group. Predisposing factors for cerebral ye-
nous thrombosis in this group (sepsis, congenital
heart disease, coagulopathy, and electrolyte dis-
turbance) were identified in 5 of the 10 infants with
thalamic hemorrhage/intraventricular hemorrhage
(patients 1, 2, 6, 10, 11).
Neurologic Outcome
The neurologic sequelae at 18 months of age are
summarized in Table 3. One infant with intraven-
tricular hemorrhage which probably originated
from choroid plexus also sustained severe birth
asphyxia and died during the neonatal period. The
incidence of developmental delay, hydrocephalus,
and seizures that persisted beyond 6 months of
age was similar in infants with thalamic hemor-
at Viet Nam:AAP Sponsored on February 10, 2014pediatrics.aappublications.orgDownloaded from
TABLE 2. Clinical Features of Full-Term Infants With Thalamic Hemorrhage/Intraventricular Hemorrhage
Source and Sex and Age Major Clinical Radiologic
Perinatal/
Patient No. Birth Wt
(g)
(d) Features Findings Postnatal
Complications
Present study
1 M, 3000 12 Vomiting, lethargy, sei- LTH/IVH, nonopaci- Urinary tract in-
zures fication of internal fection
cerebral vein (by
angiogram)
2 M, 2970 14 Irritability, focal sei- RTH/IVH, decreased Urinary tract in-
zures attenuation in thal- fection
amus
3 F, 2970 6 Opisthotonus, seizures RTH/IVH, normal None
angiogram
4 M, 3320 26 Seizures, irritability, LTH/IVH Pregnancy-induced
tense fontanelle hypertension
5 M, 2890 25 Apnea, vomiting, coma LTH/IVH None
6 M, 2890 27 Lethargy, vomiting, RTH/IVH, normal Hyponatremia, vi-
gastrointestinal hem- angiogram tamin K defi-
orrhage ciency
7 F, 3140 0.5 Apnea, focal seizures LTH/IVH, decreased None
attenuation in thal-
amus
8 M, 3750 6 R focal seizures LTH/IVH, increased Heavy meconium-
attenuation vein of stained liquor,
Galen normal Apgar
scores
9 M, 3870 2 Seizures, respiratory Bilateral TH/IVH Asphyxia, cyanotic
arrest congenital heart
disease
10 F, 3280 5 Seizures, apnea RTH/IVH Polycythemia
11 F, 3170 8 Vomiting, coma RTH/IVH, increased Sepsis
attenuation in
straight sinus
12 M, 2970 5 Seizures, apnea LTH/IVH, decreased None
attenuation in thal-
amus
Palma et al#{176}
13 M, 3250 7 R focal seizures LTH/IVH Prolonged labor,
normal Apgar
scores
14 M, 3500 26 Opisthotonus, tense LTH/IVH Prolonged rupture
fontanelle of membranes
Mitchell and O’Tuama3
15 F, 3850 12 Vomiting, dehydration, LTH/IVH None
tense fontanelle
Trounce et a14
16 F, 3110 11 Vomiting, dehydration, LTH/IVH None
tense fontanelle
17 M, 3000 14 Focal seizures, irritabil- RTH/IVH None
ity
18 F, 3260 12 Vomiting, opistho- RTH/IVH None
tonus, sunsetting
eyes
19 M, 2950 13 Generalized seizures, RTH/IVH None
opisthotonus, abnor-
mal eye movements
Primhak and Smith#{176}
20 M, 3340 1.5 Focal seizures, apnea, LTH/IVH Prolonged labor
feeding problems
* Abbreviations: R, right; L, left; TH, thalamic hemorrhage; IVH, intraventricular hemorrhage.
rhage/intraventricular hemorrhage compared with with thalamic hemorrhage/intraventricular hem-
infants with intraventricular hemorrhage from orrhage compared with infants with intraventricu-
other sources. The incidence of cerebral palsy, usu- lar hemorrhage from other sources (P < .05), how-
ally hemiparesis, was significantly higher in infants ever. Only a small minority of infants with thalamic
740 THALAMIC HEMORRHAGE AND NEWBORN
at Viet Nam:AAP Sponsored on February 10, 2014pediatrics.aappublications.orgDownloaded from
TABLE 3. Neurologic Outcome at 18 Months of Age*
ARTICLES 741
Neurologic Infants With Infants With P
Outcome Germinal Matrix!
Intraventricular
Hemorrhage and
Choroid Plexus!
Intraventricular
Hemorrhage
(n = 7)
Thalamic
Hemorrhage!
Intraventricular
Hemorrhage
(n = 12)
Values
Normal 0 2 .51
Developmental delay
Mild/moderate 5 9 .99
Severe 1
1 .99
Hydrocephalus 2
7 .35
Seizures (after 1 mo of age) 4
8 .99
Cerebral palsyt
2 10 .05t
Death 1
0 .37
* Germinal matrix/intraventricular hemorrhage + choroid plexus/intraventricular hemorrhage and thalamic hemor-
rhage/intraventricular hemorrhage were compared using the two-tailed version of Fisher’s exact test.
1 P < .05 denotes statistically significant difference between groups.
hemorrhage/intraventricular hemorrhage (2 pa-
tients) appeared normal neurologically at follow-
up. In the majority (10 patients), there was at least
mild or moderate developmental delay.
DISCUSSION
Intraventricular hemorrhage is an uncommon
problem in the full-term newborn. In contrast to
the premature newborn, in whom intraventricular
hemorrhage originates almost exclusively from sub-
ependymal germinal matrix, the origin of intraven-
tricular hemorrhage in the full-term infant is more
diverse.13 According to our data, extension of tha-
lamic hemorrhage may be the most common cause
of intraventricular hemorrhage in the full-term
newborn, an observation that has not been reported
previously in this age group.
The pathogenesis of thalamic hemorrhage/intra-
ventricular hemorrhage in the full-term newborn is
not clear. Hemorrhage into thalamus and basal
ganglia has been described previously in the full-
term newborn in association with coagulation
disorders1 and hypoxic-ischemic cerebral injury.47
In such instances, the thalamic and striatal hem-
orrhage was bilateral and was not associated with
intraventricular hemorrhage. Several isolated cases
have been reported of unilateral thalamic hemor-
rhage associated with intraventricular hemorrhage
in full-term newborns who appeared otherwise
healthy.2’3’8’9 In these instances, because of the close
proximity of large venous channels to the ventric-
ular wall, the intraventricular hemorrhage was con-
sidered to represent a secondary phenomenon re-
sulting from extension of the thalamic hemorrhage.
Thalamic hemorrhage has been described in
adults and older children in the context of chronic
hypertension.10” Similarly, in studies in both ex-
perimental animals12 and human infants a role was
suggested for intermittent episodes of hypertension
in the genesis of intraventricular hemorrhage in the
newborn.13”4 Hypertension was not observed in our
patients, however. Furthermore, although thalamic
hemorrhage has been documented in the context of
hypoxic-ischemic cerebral injury,47 a role for birth
asphyxia was not supported by the high Apgar
scores, lack of other evidence of perinatal asphyxia,
and late appearance of hemorrhage ie, often after 1
week of age. The possibility of hemorrhage from a
vascular malformation cannot be excluded entirely
in our patients (cerebral angiography was not per-
formed in all infants because of its potential mor-
bidity in this age group). The absence of vascular
abnormalities or recurrent hemorrhage on follow-
up CT scans argues against this possibility, how-
ever.
The clinical appearance of thalamic hemorrhage!
intraventricular hemorrhage was characterized by
sudden onset of marked neurologic abnormalities
in all patients. The clinical features, with the ex-
ception of timing of onset of problems, were gen-
erally nonspecific and did not permit diagnosis of
the location of hemorrhage. Thus, the clinical pres-
entation was similar to that observed in full-term
infants with intraventricular hemorrhage of other
origin and consisted principally of signs of in-
creased intracranial pressure, seizures, and dimin-
ished level of consciousness. In a recent report8 of
4 full-term newborns with thalamic hemorrhage!
intraventricular hemorrhage, persistent downward
deviation of the eyes was observed in two infants.
The authors speculated that this clinical feature
may be pathognomonic of hemorrhage in this lo-
cation. We did not observe this sign in any of our
patients with thalamic hemorrhage/intraventricu-
lar hemorrhage, however. Late onset of clinical
abnormalities, ie, often after 4 days of age, in as-
sociation with an uneventful birth history occurred
at Viet Nam:AAP Sponsored on February 10, 2014pediatrics.aappublications.orgDownloaded from
742 THALAMIC HEMORRHAGE AND NEWBORN
in the majority of cases of thalamic hemorrhage!
intraventricular hemorrhage (17 of 20 patients).
The clinical abnormalities of late onset appear to
be characteristic of this condition. This suggests
that thalamic hemorrhage/intraventricular hemor-
rhage may be a result of postnatal causes. Predis-
posing factors for venous thrombosis (sepsis, con-
genital heart disease, and hematologic disturb-
ances) were documented in 6 of the 12 infants with
thalamic hemorrhage/intraventricular hemorrhage
in our study.
Although the diagnosis of thalamic hemorrhage!
intraventricular hemorrhage in our patients was
made radiologically on the basis of CT findings, it
may also be established by cranial ultrasonog-
raphy.6’7 In three infants in whom thalamic hem-
orrhage was less extensive, there was decreased
tissue attenuation in the thalamus adjacent to the
hemorrhage in the CT scans, which is consistent
with hemorrhagic infarction in that region (Fig 2).
Furthermore, the observation of increased atten-
uation in the region of the straight sinus on CT
scans of two infants with thalamic hemorrhage/
intraventricular hemorrhage performed without
contrast enhancement (Fig 1), as well as the ab-
sence of opacification of the ipsilateral internal
cerebral vein during cerebral angiography in one
patient (Fig 3), raises the possibility that venous
occlusion may play a role in the pathogenesis of
hemorrhagic thalamic infarction.15’16 An associa-
tion between thrombosis of the internal cerebral
vein and hemorrhagic thalamic infarction has been
demonstrated previously by neuropathologic stud-
ies in young infants. Intraventricular hemorrhage
was not uncommon, presumably because of the
proximity of the larger venous channels to the
ventricular walls.17
Except for a significantly greater incidence of
cerebral palsy in infants with thalamic hemor-
rhage/intraventricular hemorrhage, the outcome of
these patients did not differ significantly from that
of infants with intraventricular hemorrhage from
other sources. A variable neurologic outcome was
suggested in previous reports3’8’9 of infants with
unilateral thalamic hemorrhage/intraventricular
hemorrhage. In contrast, infants with bilateral tha-
lamic hemorrhage following birth asphyxia have
uniformly poor prognosis and have either died or
developed severe neurologic sequelae.47 According
to our data, neurologic sequelae, eg, hydrocephalus,
seizures, and cerebral palsy (especially hemiplegia),
are common following thalamic hemorrhage/intra-
ventricular hemorrhage and occur in the majority
of cases. Only a minority of infants appeared neu-
rologically and developmentally normal at 18
months of age.
In summary, a high incidence of thalamic hem-
orrhage is suggested by our data as a cause of
intraventricular hemorrhage in the full-term new-
born. This is seen especially in infants with Un-
eventful birth histories and infants in whom clinical
abnormalities develop after 1 week of age. Both the
clinical appearance during the newborn period and
neurologic outcome appear similar to that of full-
term infants with intraventricular hemorrhage
originating from other sites. Thus, although tha-
lamic hemorrhage/intraventricular hemorrhage
may be suspected on the basis of clinical features,
definitive diagnosis is based on radiologic abnor-
malities observed either on CT scans, cranial ultra-
sonography, or cerebral angiography.
REFERENCES
1. Volpe JJ. Neurology of the Newborn. Philadelphia, PA: WB
Saunders Co; 1987
2. Palma PA, Miner ME, Morriss FH, et al. Intraventricular
hemorrhage in the neonate born at term. Am J Dis Child.
1979;133:941-944
3. Mitchell W, O’Tuama L. Cerebral intraventricular hemor-
rhages in infants: a widening age spectrum. Pediatrics.
1980;65:35-39
4. Kotagal 5, Toces 5, Kotagal P, Archer C. Symmetric hi-
thalamic and striatal hemorrhage following perinatal hy-
poxia in a term infant. J Comput Assist Tomogr.
1983;17:353-355
5. Voit T, Lemburg P. Damage of thalamus and basal ganglia
in asphyxiated full-term neonates. Neuropediatrics. 1987;
18:176-181
6. Kreusser KL, Schmidt RE, Shackelford GD, Volpe JJ. Value
of ultrasound for identification of acute hemorrhagic necro-
sis of thalamus and basal ganglia in an asphyxiated term
infant. Ann Neurol. 1984;16:361-363
7. Donn SM, Bowerman RA, DiPietro MA, Gebarski S. Son-
ographic appearance of neonatal thalamic-striatal hemor-
rhage. J Ultrasound Med. 1984;3:231-233
8. Trounce JQ, Dodd KL, Fawer C-L, Fielder AR, Punt J,
Levene MI. Primary thalamic haemorrhage in the newborn:
a new clinical entity. Lancet. 1985;1:190-192
9. Primhak RA, Smith MF. Primary thalamic hemorrhage in
first week of life. Lancet. 1985;1:635
10. Waishe TM, David KR, Fisher CM. Thalamic hemorrhage:
a computed tomographic-clinical correlation. Neurology.
1977;27:217-’222
11. Livingston JH, Brown JK. Intracerebral haemorrhage after
the neonatal period. Arch Dis Child. 1986;61:538-544
12. Goddard J, Lewis RM, Armstrong DL, Zeller RS. Moderate,
rapidly induced hypertension as a cause of intraventricular
hemorrhage in the newborn beagle model. ,J Pediatr.
1980;96:1057-1060
13. Wimberley PD, Lou HC, Pedersen H, et al. Hypertensive
peaks in the pathogenesis of intraventricular hemorrhage in
the newborn: abolition by phenobarbitone sedation. Acta
Pediatr Scand. 1982;71:537-542
14. Young RSK, Liberthson RR, Zalneraitis EL. Cerebral hem-
orrhage in neonates with coarctation of the aorta. Stroke.
1982;13:491-494
15. Wendling LR. Intracranial venous sinus thrombosis: diag-
nosis suggested by computed tomography. Am J Roentgenol.
1978;130:978-980
16. Rao KC, Knipp HC, Wagner EJ. Computed tomographic
findings in cerebral sinus and venous thrombosis. Radiology.
1981;140:391-398
17. Ehlers H, Courville CB. Thrombosis of internal cerebral
veins in infancy and childhood: Review of literature and
report of five cases. J Pediatr. 1936;8:600-623
at Viet Nam:AAP Sponsored on February 10, 2014pediatrics.aappublications.orgDownloaded from
1990;85;737Pediatrics
Elke H. Roland, Olof Flodmark and Alan Hill
Thalamic Hemorrhage With Intraventricular Hemorrhage in the Full-Term Newborn
Services
Updated Information &
/>including high resolution figures, can be found at:
Citations
/>This article has been cited by 3 HighWire-hosted articles:
Permissions & Licensing
/>or in its entirety can be found online at:
Information about reproducing this article in parts (figures, tables)
Reprints
/>Information about ordering reprints can be found online:
Online ISSN: 1098-4275.
Copyright © 1990 by the American Academy of Pediatrics. All rights reserved. Print ISSN: 0031-4005.
American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village, Illinois, 60007.
has been published continuously since 1948. PEDIATRICS is owned, published, and trademarked by the
PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly publication, it
at Viet Nam:AAP Sponsored on February 10, 2014pediatrics.aappublications.orgDownloaded from
