Pediatr Radiol (1992) 22:123-127

Pediatric
Radiology
9 Springer-Verlag 1992

Deep cerebral venous thrombosis in thalamo-ventricular
hemorrhage of the term newborn
P. G o v a e r t 1, E. A c h t e n 2, P. V a n h a e s e b r o u c k I, C. D e Praeter 1, and J. V a n D a m m e 3

1Department of Pediatrics and
2Department of Radiology, Gent University Hospital, Gent, Belgium
3Department of Pediatrics, A Z Maria Middelares, Kortrijksestwg 1026, Gent, Belgium
Received: 20 September 1991; accepted: 26 September 1991

Abstract. U n i l a t e r a l t h a l a m i c b l e e d i n g with a s s o c i a t e d int r a v e n t r i c u l a r h e m o r r h a g e is r e p o r t e d in t h r e e f u l l - t e r m
n e o n a t e s . T h e first p r e s e n t e d w i t h i n 48 h o u r s f r o m b i r t h
with e a r l y o n s e t s t r e p t o c o c c a l meningitis, p e r s i s t e n t pulm o n a r y h y p e r t e n s i o n , t o n i c seizures a n d a t e n s e f o n t a nelle. T h e s e c o n d p r e s e n t e d 6 d a y s a f t e r b i r t h with irritability, o p i s t h o t o n u s , a t e n s e f o n t a n e l l e a n d t o n i c seizures.
T h e t h i r d was a d m i t t e d t h r e e days a f t e r b i r t h with seizures
a n d a t e n s e f o n t a n e l l e . I n t h e la~tter two infants N M R a n d
C T i m a g i n g d o c u m e n t e d t h r o m b o s e d superficial a n d
d e e p c e r e b r a l veins. T h e e t i o p a t h o g e n e s i s of i n t r a c r a n i a l
v e n o u s t h r o m b o s i s in the n e o n a t e is diverse: asphyxia, deh y d r a t i o n , p o l y c y t h e m i a , s e p s i s - m e n i n g i t i s a n d difficult
d e l i v e r y a r e the m a i n causes. I n o n e o f o u r p a t i e n t s j u g u l a r
v e i n c o m p r e s s i o n b y t h e collar of a n e g a t i v e - p r e s s u r e
ventilation chamber probably initiated the intracranial
events. M o r e t h a n half o f t h e survivors sustain s e v e r e
neurological impairment.

B l e e d i n g into t h e b a s a l g a n g l i a of the n e w b o r n can b e ass o c i a t e d w i t h a m y r i a d of events: s e v e r e b i r t h a s p h y x i a [12,
18], g e n e r a l i z e d h e m o r r h a g i c diathesis [15], e x t e n s i o n
f r o m a g e r m i n a l l a y e r h e m o r r h a g e o r f r o m a c h o r o i d plexus b l e e d i n g in t h e l a t e r a l o r t h i r d ventricle [5], b l e e d i n g
f r o m a m i c r o - a n g i o m a [1, 19], o r into an i n t r a c r a n i a l
t u m o r [15]. T h e e v e n t o f a u n i l a t e r a l t h a l a m i c h e m o r r h a g e
with o r w i t h o u t i n t r a v e n t r i c u l a r clot f o r m a t i o n , has b e e n
r e c o g n i z e d s p o r a d i c a l l y in t h e at o r n e a r t e r m n e w b o r n
since t h e a d v e n t of CT. F r o m p e r s o n a l e x p e r i e n c e with
3 r e c e n t o b s e r v a t i o n s a n d a r e v i e w on 22 i n s t a n c e s f r o m
the l i t e r a t u r e , w e p r o p o s e d e e p c e r e b r a l v e n o u s t h r o m bosis as t h e m a i n e t i o p a t h o g e n e t i c m e c h a n i s m of this old
clinical s y n d r o m e [6].

Case reports
First case (BW, 89/2534, ~

Following an uneventful pregnancy this girl was born at term by
spontaneous vaginal delivery. The membranes had ruptured one
week earlier, but oligohydramnios and clinical chorioamnionitis

were absent. Her birthweight was 3430 g for a length of 49 cm and a
head circumference of 34 cm. The Apgar scores were 9 at i and at
5 minutes. Well into the second day of life the girl started grunting
and became tachycardic. Because of increasing cyanosis, a tense fontanelle and generalized tonic seizures a septic screen was done, revealing purulent meningitis. After referral to our Neonatal Intensive
Care Unit she was noted to have anisocoria (right pupil larger than
left) and presented with obvious tonic seizures besides subtle convulsions. Her metabolic acidosis, hypotension and neutropenia were
successfully treated but seizures persisted for 9 days despite phenobarbital, diphenylhydantoin, paraldehyde and diazepam. The lowest
serum calcium was 5,8 mg/dL, but she was never hypoglycemic. Near
the end of the first week a transient mild thrombocytopenia was documented. Blood and CSF cultures both grew Streptococcus agalactiae. After an initial period of persistent pulmonary hypertension
with corresponding ventilatory treatment, she was slowly weaned
from the ventilator 2 weeks after admission. It took i week to switch
from nasogastric to oral feeding. On day 16 of life she had an EEG
recording which showed epileptical activity covering the whole left
hemisphere. Her eye grounds were unremarkable. Serial ultrasound
examinations revealed a unilateral thalamic bleeding with minor intraventricular clot formation on the same side (Fig. 1). A C T scan
was delayed for practical reasons until day 16 (Fig. 2). At the end of
the first month she was hypotonic with bilateral ankle clonus. Her
right pupil remained unresponsive to light and mydriatic for
2 months. In the absence of maintenance anticonvulsant therapy her
EEG had a good structural basis on day 30, with intercurrent runs of
irritative slow wave activity without persistent lateralisation. At the
age of 6 months she was slightly hypotonic and had a high pitched
cry, but was not suffering from cerebral palsy and found to be appropriate for age on a Denver Developmental Screening test. The thalamic density had disappeared on ultrasound in the beginning of the
second month, not leaving a posthemorrhagic hydrocephalus.

S e c o n d case ( V L L , 90/754, ~

This boy presented in breech position at term, following an unremarkable pregnancy. Delivery of the aftercoming head created some
difficulty: the chin was locked behind the symphysis and a rotational
manoeuver was necessary before proceeding to delivery according
to Mauriceau. He weighed 3100 g for a length of 49 and a head
circumference of 34 cm. The Apgar scores were 5 and 9 at 1 and
5 minutes. His postnatal course was uneventful until the sixth day of
life. Irritability, opisthotonic posturing and a tense fontanelle
preceded sudden generalised tonic seizures. He had a high pitched
cry and started vomiting. Following an ultrasound examination he
was referred to our Neonatal Intensive Care Unit. Upon admission
his pupils were symmetrically responsive to light and isocoric. Tran-

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Fig.la, b. (first patient) US scan of the brain (7.5 MHZ) on day 3:
acoronal section behind the foramina of Monro: hemorrhagic
density within the left thalamo-caudate region (arrows); limited
ventricular clot formation (arrowhead). b left parasagittal section:
density restricted to upper left thalamus (T) in front of the choroid
plexus (CP) and behind the nucleus caudatus (NC) (arrows); intraventricular clot (arrowhead)
Fig.2. (first patient) uncontrasted CF scan of the brain on day 16:
spontaneous opacification within the great cerebral vein (arrowhead); hemorrhagic opacities in the left basal ganglia (arrows)

sient right facial palsy was noticeable together with lateroflexion of
the head due to bleeding within the right sternocleidomastoidus
muscle. The seizures subsided with loading doses of phenobarbital
and diphantoin. A thorough coagulation screen was normal except
for a fibrinogen level of 99 mg/dL with a normal platelet count. US
demonstrated a large bleed within the left thalamus, bilateral intraventricular bleeds and suspected white matter ischemia around
the left lateral ventricle (Fig. 3). The hemorrhagic mass crossed the
midline. High frequency sonographic scanning (10 MHZ) through
the posterior fontanelle suggested limited densities within the tip of
the superior sagittal sinus but on Colour Doppler flow imaging the
vessel showed presence of venous flow. An uncontrasted CT scan the
same day revealed additional spontaneous densities within the torcular Herophili and the great cerebral vein of Galen besides the
bleeding suspected on ultrasound (Fig. 4). One week later an NMR
scan documented extensive thromboses within the superior sagittal
sinus, the straight sinus and several deep cerebral venous structures
(Fig. 5). It confirmed unilateral white matter changes. At the age of
5 months he had mild spastic diplegia.

Third case ( G O , 91/58, ~
This boy was born after a pregnancy of 36 weeks complicated by preeclampsia. Oligohydramnios and fetal growth retardation had been
recognized with prenatal echography. Following onset of labor, oxytocin augmentation was started. The delivery was spontaneous vaginal with a second stage of 20 minutes. The cord was tightly wrapped
twice around the neck. His birthweight was 2000 g for a length of 43
and a head circumference of 33 cm respectively. Apgar scores were
4 and 6 at 1 and 5 minutes. The remaining liquor was meconium
stained. Because of respiratory difficulties the newborn was nursed
in a negative-pressure respirator [10] and received parenteral antibiotic treatment with ampicillin and netromycin. Despite an uneventful recovery on the first day of life sudden fever (39,5 ~
paleness and obvious generalized tonic seizures necessitated
endotracheal ventilation and referral to our Neonatal Intensive Care
Unit on day 2. On admission tonic and clonic seizures were noticed.
The fontanelle was tense. There were no abnormal eye movements.
In the neck a single deep and hemorrhagic pressure mark was pre-

sent on the right side: we felt this to be compatible with a local injury
by the ventilator collar (Fig. 6). Hemoglobin in blood was 12.3 g/dL,
platelets were 44.000/mm 3 and fibrinogen 111 mg/dL. Lumbar CSF
was uniformly hemorrhagic and did not clot. The clinical evolution
excluded early onset septicemia. US scan on the third day of life disclosed bilateral intraventricular bleeding with extension of the
coagulum into the right intercaudo-thalamic fissure; both the left
and especially the right periventricular white matter contained
cloudy echodensities suggestive of severe ischemia (Fig. 7). CT and
NMR scan on day 4 revealed additional densities within the straight
sinus, the occipital and transverse sinus and several cerebral bridging
veins, corresponding to venous thrombi (Fig. 8). His clinical course
went downhill with obvious bilateral leucomalacia on US scan and
cerebral atonia preceding neonatal death on day 14.

Discussion
I n c l u d i n g t h r e e d e s c r i b e d h e r e , 25 instances of t h a l a m o v e n t r i c u l a r b l e e d i n g in at or n e a r t e r m n e w b o r n s w e r e
reviewed [11, 14, 15, 17, 20]. A l l h a d a b i r t h w e i g h t a b o v e
2000 g ( m e a n 3078). S e v e n t e e n w e r e m a l e (68 % ) . B i r t h
t r a u m a was r e s p o n s i b l e for the e v e n t in 4 infants, b i r t h asp h y x i a c o n t r i b u t e d in a n o t h e r 4. D e l i v e r y was s p o n t a n e o u s v a g i n a l in 8, with low o u t l e t f o r c e p s in 2, b y c a e s a r e an s e c t i o n in i a n d b y t h e b r e e c h in still a n o t h e r (no d a t a in
13 n e o n a t e s ) . P r o b a b l e e t i o p a t h o g e n e t i c factors w e r e d e h y d r a t i o n in 3, h y p o n a t r e m i a in 1, p o l y c y t h e m i a in 1, sepsis in 3, m e n i n g i t i s in i (case I in this r e p o r t ) , h e m o r r h a g i c
diathesis in 2 a n d j u g u l a r v e i n c o m p r e s s i o n in 1 (case 3 in
this r e p o r t ) . T h e clinical f e a t u r e s a r e g a t h e r e d in T a b l e 1.
I n 1979 P a l m a et al. r e p o r t e d on 2 f u l l - t e r m n e o n a t e s
with C T - c o n f i r m e d i n t r a v e n t r i c u l a r h e m o r r h a g e a n d ass o c i a t e d b l e e d i n g in t h e b a s a l g a n g l i a on o n e side [15].
B o t h p r e s e n t e d s e v e r a l d a y s f r o m b i r t h with an acute
n e u r o l o g i c a l d e t e r i o r a t i o n n o t r e l a t e d to b i r t h a s p h y x i a o r
infection. T h e a u t h o r s s u g g e s t e d t h e o c c u r r e n c e of del a y e d g e r m i n a l m a t r i x b l e e d i n g , in o n e infant p r o b a b l y
facilitated b y v i t a m i n K deficiency. A few m o n t h s l a t e r
M i t c h e l l a n d O ' T u a m a w i d e n e d t h e age s p e c t r u m of int r a v e n t r i c u l a r h e m o r r h a g e f r o m t h e n e o n a t a l to t h e infantile p e r i o d [14]. In a n e w b o r n girl t h e y d e t a i l e d a t h a l a m o v e n t r i c u l a r b l e e d o n d a y 12. A four-vessel a n g i o g r a m at
20 days of age r e v e a l e d a n o r m a l a r t e r i a l a n d superficial
c e r e b r a l v e n o u s p h a s e , b u t failed to visualise t h e d e e p
c e r e b r a l v e n o u s system. T h e s e a u t h o r s chose t h e e p o n y m
" s p o n t a n e o u s " to d e s c r i b e the event, b u t o b v i o u s d e h y d r a t i o n m a y h a v e b e e n an e t i o l o g i c a l factor. T h e y specu-

125
Fig.3a-d. (second patient) US scan of the brain
(7.5 MHZ) on day 7:
a coronal section behind the foramina of Monro:
hemorrhage within the left basal ganglia (arrows);
bilateral ventricle clots (arrowheads)
b sagittal section: the density crosses the midline
(arrow) (V4 = fourth ventricle, CC = corpus callo-

sum)

e left parasagittal section: large intrathalamic density
(arrows); intraventricular hemorrhage (arrowhead)
d left parasagittal section through centrum semiovale: hemorrhage in lateral basal ganglia (arrows);
fluffy densities in the occipital periventricular white
matter (arrowheads)
Fig.4.a,b. (second patient) uncontrasted CTscan of
the brain on day 7:
a section at the level of the basal ganglia: parasagittal
hemorrhage mainly filling the left thalamic region
and crossing the midline (arrows)
b section through the temporal horns of the lateral
ventricles: hemorrhage within the left ventricle; spontaneous opacification of the great cerebral vein
(GCV) and superior sagittaI sinus (arrowheads)
Hg.5a-e. (second patient) NMRimages of thebrain
on day 14:
a left para-sagittal section (Tl-weighted): increased
signal intensity within the superior sagittal sinus
(SSS), sinus rectus (SR), great cerebral vein (GCV),
left thalamus (T) and left lateral ventricle (LLV); central less intense zones are characteristic of clot formation (arrows)
b axial section (Tl-weighted): irregular signals of increased intensity in the superior sagittal sinus (arrowhead) and the left frontoparietal supraventricular
white matter (arrows)
c axial section (Tl-weighted) through the great cerebral vein (GCV): note the curvilinear high signal
streaks sprouting from the thrombosed GCV (arrowheads) (possibly the internal cerebral veins and the
basal vein of Rosenthal), the high signal intensity in a
linear structure within the lateral ventricle (arrow)
(choroid plexus vein), an ovoid hypersignal in the
right parieto-temporal subarachnoid space (asWrisk)
(superficial cerebral vein or anastomosing vein of
Labbd).

126

Fig.6. (thirdpatient):nuchalinjuryfroman overtightseal by the collar of a negative-pressureventilator
Fig.7. (third patient) US scanof the brain on day 3: intraventricular
clot extendingbetweenthalamus and caput nucleicaudati (arrows);
periventricularwhitematter ischemia(asterisk)
Fig.8. (third patient) Tl-weighted NMR image of the brain on
day 4: intravascularclots in the occipitaland straightsinus (arrows)
and in a cerebral bridgingvein (arrowhead)
lated that, at least in some children, bleeding may originate in the choroid plexus as suggested in autopsy reports
[5]. Trounce et al. accounted for 4 full-term newborns with

unilateral thalamic hemorrhage presenting unexpectedly
in the second week of life [20]. Their main contribution
was to specify the associated ophthalmological findings,
possibly due to damage of the subthalamic frontomesencephalic optic pathway: vertical upward gaze palsy, deviation of the eyes towards the lesion, ipsilateral saccadic
paresis and/or a flat visual evoked response. Three of the
infants suffered from residual cerebral palsy and two
needed ventriculoperitoneal shunting. In the discussion it
was stipulated that one should differentiate this "new
clinical entity" of unilateral thalamic bleeding from bilateral hemorrhagic infarction of the basal ganglia following
severe birth asphyxia [12]. The first NMR images on this
topic were reported in a dehydrated infant with extensive
thrombosis of intracranial veins following misplacement
of a central catheter up into the jugular vein [11]. The association with thalamic bleeding suggested deep cerebrovenous thromboses not shown in the figures of this report. A comprehensive review of in vivo diagnosed
thalamo-ventricular hemorrhage in the full-term newborn
is provided by Roland et al. [17]. At British Columbia
Children's Hospital they recognized 19 instances of intraventricular hemorrhage diagnosed with CT and US
scan in full-term neonates born between 1980 and 1987
and less than one month old. Twelve of these lesions were
judged to follow a primary thalamic hemorrhage, 3 were
thought to originate in residual germinal matrix and in 4
an undefinite source was suggested. The "thalamic" variety of intraventricular hemorrhage manifested mainly
after the first 48 hours (10 of their 12 personal observations) whereas the "germinal matrix" variety invariably
presented on the first or second day of life. In about half of
their patients no etiological explanation was possible. Angiographic studies, normal in 2 neonates, disclosed impossible opacification of the deep venous system in one infant, despite absence of abnormal attenuation of the
straight sinus on uncontrasted CT scan in this child. Only
a minority of infants recovered completely.
Already in 1936 Ehlers and Courville summarized
clinical and pathological findings on 26 children with deep
cerebral venous thrombosis, including 5 of their own [6].
Three of those children were newborn. Both the existence
of an association thalamic hemorrhage-ventricular bleeding and of an association deep venous thrombosisthalamic hemorrhage was recognized. Throughout subsequent years a multitude of etiopathogenetic mechanisms
were gradually associated with deep cerebral venous
thrombosis in newborn infants (Table 2). An extensive
amount of reports have documented the occurrence of
deep venous thrombosis following difficult delivery.
Nevertheless, the complete picture of bilateral thalamoventricular bleeding and a thrombosed, saccular and aneurysmal great cerebral vein of Galen has become a rare
event in modern perinatology, probably due to the virtual
disappearance of very prolonged labour [16]. On the other
hand, this old concept of deep venous stasis in intracranial
veins gained new interest in the study of germinal layer
hemorrhage in preterm infants [23]. Several case reports
mentioned the probable contribution of dehydration to
thalamic hemorrhage [3]. Our first patient confirms the
possibility of deep thrombophlebitis associated with men-

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Table 1.

Thalamo-ventricular bleeding in the full-term neonate.

Clinicalfeatures (22 literature + 3 personal observations)
n = 25
Free interval from birth (days)
9 mean
9 range
9 _> 8 / > 15
9 <1/<7

11
1-27
13/5
3/12

Signs and symptoms
9 lethargy/irritability
9 opisthotonus
9 fontanelle: bulging/normal
9 seizures: focal/general
9 contralateral hemiparalysisa
9 high pitched cry
9 eye signs - sunsetting
- nystagmus
- saccadic paresisb
Neonatal death
Hydrocephalus requiring shunt
Normal survival
Cerebral palsy

4/10
6
7/2
8/9
3
3
5
1
3
2
12
6
14

except for one ipsilateral instance
b ipsilateral [20]
Table 2. Etiology of deep cerebral venous thrombosis in the neonate

9 Following difficult delivery
9 Primary (marantic) thrombosis due to dehydration [3]
9 Associated with leptomeningitis and ventriculitis [2, 7]
9 In association with cyanotic heart disease and polycythemia
[4, 13]
9 As a consequence of thrombosis in a major superficial cerebral
vein or sinus, extending into deeper vessels via the straight
sinus [3]
9 Following severe birth asphyxia [22]
9 In the vicinity of a germinal layer hemorrhage [8]

ingitis [2, 7]. Polycythemia, as in n e o n a t e s with c y a n o t i c
h e a r t disease, is a w e l l k n o w n cause of v e n o u s occlusion
a n d t h e case p r e s e n t e d b y M i l l e r et al. is f i r m l y suggestive
of t h a l a m i c b l e e d i n g following p o l y c y t h e m i a [13]. A l l etiological factors l e a d i n g to superficial cerebral venous
thrombosis in t h e n e o n a t e , are i n d i r e c t causes o f d e e p
c e r e b r o v e n o u s t h r o m b o s i s . O n e r e p o r t suggests a n imp o r t a n t r61e f o r asphyxia in s o m e i n s t a n c e s of v e n o u s
t h r o m b o s i s w i t h i n t h e c r a n i u m [22]. Finally, a n y s e v e r e
(fatal) intraventricular bleeding m a y l e a d to h e m o r r h a g i c
v e n o u s p e r i v e n t r i c u l a r i n f a r c t i o n [8].
O u r s e c o n d case is a u n i q u e e x a m p l e of in vivo diagn o s e d deep cerebral venous thrombosis associated with
late onset thalamo-ventricular bleeding in a full-term
neonate. A n g i o g r a p h i c studies a l r e a d y s u g g e s t e d this
p h e n o m e n o n b e f o r e [14, 17]. E v i d e n t l y the p o s t m o r t e m
o b s e r v a t i o n s r e f e r r e d to a b o v e firmly u n d e r s c r i b e this
cause a n d effect r e l a t i o n [6]. A s t h e c o r p u s striatum, d o r s a l
t h a l a m u s , c h o r o i d p l e x u s a n d s u b e p e n d y m a l m a t r i x at
the f o r a m e n o f M o n r o a r e all d r a i n e d b y t h e i n t e r n a l
c e r e b r a l veins, occlusion of t h e s e vessels o r t h e i r t r i b u t a t r i e s c a n l e a d to d e e p h e m o r r h a g i c i n f a r c t i o n a n d / o r germinal layer bleeding and/or choroid plexus hemorrhage,
e x p l a i n i n g t h e f r e q u e n t a s s o c i a t i o n of b l e e d i n g i n t o t h e
b a s a l g a n g l i a with i n t r a v e n t r i c u l a r h e m o r r h a g e [6,14,15].

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E Govaert
Neonatal Intensive Care Unit
Gent University Hospital
De Pintelaan 185
B-9000 Gent, Belgium