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The Radiology Assistant

Cerebral Venous Thrombosis


by Barbara Simons, Geert Lycklama a Nijeholt and Robin Smithuis
Radiology department of the Medical Centre Haaglanden in the Hague and the Rijnland hospital in Leiderdorp, the Netherlands
Introduction
When to think of venous thrombosis
Dense clot sign
Empty delta sign
Absence of normal flow void on MR
Venous infarction
Imaging in suspected thrombosis
CT-venography
MR-venography
DSA
Pitfalls in CT
Arachnoid Granulations
Pseudodelta sign
Wrong bolus timing
Hematoma simulating venous thrombosis
Pitfalls in MRI
Hypoplastic transverse sinus
Low signal intensity in thrombus
Flow void on contrast-enhanced MR
Chronic dural sinus thrombosis and related
syndromes
DAVF
Thrombosis and increased CSF pressure
Venous territories
Publicationdate:21-10-2010
Cerebral venous thrombosis is an important cause of
stroke especially in children and young adults.
It is more common than previously thought and
frequently missed on initial imaging.
It is a difficult diagnosis because of its nonspecific
clinical presentation and subtle imaging findings.
In this article we will focus on:
Findings on routine imaging that should make
you think of unsuspected venous thrombosis.
How to image patients in suspected venous
thrombosis.
Pitfalls.
You can enlarge images by clicking on them.
This item is not available on the iPhone application.
Introduction
Cerebral venous thrombosis is located in descending
order in the following venous structures:
Major dural sinuses:
Superior sagittal sinus, transverse, straight and
sigmoid sinuses.
Cortical veins:
Vein of Labbe, which drains the temporal lobe.
Vein of Trolard, which is the largest cortical vein
that drains into the superior sagittal sinus.
Deep veins:
Internal cerebral and thalamostriate veins.
Cavernous sinus.
Clinically patients with cerebral venous thrombosis
present with variable symptoms ranging from
headache to seizure and coma in severe cases.
In neonates shock and dehydration is a common
cause of venous thrombosis.
In older children it is often local infection, such as
mastoiditis, or coagulopathy.
In adults, coagulopathies is the cause in 70% and
infection is the cause in 10% of cases.
In women, oral contraceptive use and pregnancy are
strong risk factors.
When to think of venous thrombosis
Venous thrombosis has a nonspecific presentation and
therefore it is important to recognize subtle imaging
findings and indirect signs that may indicate the
presence of thrombosis.
Although these findings are often present on initial
scans, they are frequently detected only in retrospect.
Clinically patients with venous thrombosis often
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present with seizures, which is not a symptom in
patients with an arterial infarction.
On a routine non-enhanced MR or CT you should think
of the possibility of venous thrombosis when you see:
Direct signs of a thrombus
Infarction in a non-arterial location, especially if it is
bilateral and hemorrhagic
Cortical or peripheral lobar hemorrhage
Cortical edema
Dense clot sign
Direct visualization of a clot in the cerebral veins on a
non enhanced CT scan is known as the dense clot
sign.
It is seen in only one third of cases.
Normally veins are slightly denser than brain tissue
and in some cases it is difficult to say whether the
vein is normal or too dense (see pitfalls).
In these cases a contrast enhanced scan is necessary
to solve this problem.
Dense clot sign in a thrombosed cortical vein.
Dense clot sign (2)
Visualization of a thrombosed cortical vein that is seen
as a linear or cord-like density, is also known as the
cord sign.
Another term that is frequently used, is the dense
vessel sign.
Dense clot sign (3)
On the left images of a patient with a hemorrhagic
infarction in the temporal lobe (red arrow).
Notice the dense transverse sinus due to thrombosis
(blue arrows).
Empty delta sign
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Two cases of empty delta sign due to thrombosis of the
superior sagittal sinus.
The empty delta sign is a finding that is seen on a
contrast enhanced CT (CECT) and was first described
in thrombosis of the superior sagittal sinus.
The sign consists of a triangular area of enhancement
with a relatively low-attenuating center, which is the
thrombosed sinus.
The likely explanation is enhancement of the rich
dural venous collateral circulation surrounding the
thrombosed sinus, producing the central region of low
attenuation.
In early thrombosis the empty delta sign may be
absent and you will have to rely on non-visualization
of the thrombosed vein on the CECT.
The sign may be absent after two months due to
recanalization within the thrombus.
Empty delta sign (2)
On the left a case of thrombosis of the right
transverse sinus and the left transverse and sigmoid
sinus (arrows).
There is enhancement surrounding the thrombosed
hypoattenuating veins.
Venous thrombosis with absence of normal flow void on T2-
weighted image..
Absence of normal flow void on MR
On spin-echo images patent cerebral veins usually will
demonstrate low signal intensity due to flow void.
Flow voids are best seen on T2-weighted and FLAIR
images, but can sometimes also be seen on T1-
weighted images.
A thrombus will manifest as absence of flow void.
Although this is not a completely reliable sign, it is
often one of the first things, that make you think of
the possibility of venous thrombosis.
The next step has to be a contrast enhanced study.
On the left a T2-weighted image with normal flow void
in the right sigmoid sinus and jugular vein (blue
arrow).
On the left there is abnormal high signal as a result of
thrombosis (red arrow).
Absence of normal flow void on MR (2)
The images on the left show abnormal high signal on
the T1-weighted images due to thrombosis.
The thrombosis extends from the deep cerebral veins
and straight sinus to the transverse and sigmoid sinus
on the right.
Notice the normal flow void in the left transverse sinus
on the right lower image.
Absence of normal flow void on MR-images can be
very helpful in detecting venous thrombosis, but there
are some pitfalls as we will discuss later.
Slow flow can occur in veins and cause T1
hyperintensity.
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Venous thrombosis with absence of normal flow void on T1-
weighted image.
Venous infarction
The other sign that can help you in making the
diagnosis of unsuspected venous thrombosis is venous
infarction.
Venous thrombosis leads to a high venous pressure
which first results in vasogenic edema in the white
matter of the affected area.
When the proces continues it may lead to infarction
and development of cytotoxic edema next to the
vasogenic edema.
This is unlike in an arterial infarction in which there is
only cytotoxic edema and no vasogenic edema.
Due to the high venous pressure hemorrhage is seen
more frequently in venous infarction compared to
arterial infarction.
Since we are not that familiar with venous infarctions,
we often think of them as infarctions in an atypical
location or in a non-arterial distribution.
However venous infarctions do have a typical
distribution, as shown on the left.
Since many veins are midline structures, venous
infarcts are often bilateral.
This is seen in thrombosis of the superior sagittal
sinus, straight sinus and the internal cerebral veins.
Bilateral infarction in superior sagittal sinus thrombosis
Venous infarction (2) - Superior sagittal sinus
thrombosis
The most frequently thrombosed venous structure is
the superior sagittal sinus.
Infarction is seen in 75% of cases.
The abnormalities are parasagittal and frequently
bilateral.
Hemorrhage is seen in 60% of the cases.
On the left bilateral parasagittal edema and subte
hemorrhage in a patient with thrombosis of the
superior sagittal sinus.
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On the left reconstructed sagittal CT-images in a
patient with bilateral parasagittal hemorrhage due to
thrombosis of the superior sagittal sinus.
The red arrow on the contrast enhanced image
indicates the filling defect caused by the thrombus.
Venous infarct in Labb territory
Venous infarcts (3) - vein of Labbe
Another typical venous infarction is due to thrombosis
of the vein of Labb.
On the left images demonstrating hypodensity in the
white matter and less pronounced in the gray matter
of the left temporal lobe.
There is a broad differential diagnosis including
arterial infarction, infection, tumor etc.
Notice that there is some linear density within the
infarcted area.
This is due to hemorrhage.
In the differential diagnosis we also should include a
venous infarct in the territory of the vein of Labbe.
The subtle density in the area of the left transverse
sinus (arrow) is the key to the diagnosis.
This is a direct sign of thrombosis and the next step is
a CECT, which confirmed the diagnosis (not shown).
Hemorrhagic venous infarct in Labb territory
On the left images of a patient with hemorrhage in the
temporal lobe.
When the hemorrhagic component of the infarction is
large, it may look like any other intracerebral
hematoma with surrounding vasogenic edema.
The clue to the diagnosis in this case is seen on the
contrast enhanced image, which nicely demonstrates
the filling defect in the sigmoid sinus (blue arrow).
Hemorrhagic venous infarct in Labbe territory
On the left a similar case on MR.
There is a combination of vasogenic edema (red
arrow), cytotoxic edema and hemorrhage (blue
arrow).
These findings and the location in the temporal lobe,
should make you think of venous infarction due to
thrombosis of the vein of Labb.
The next examination should be a contrast enhanced
MR or CT to prove the diagnosis.
Venous infarction (4) - Deep cerebral veins
On the far left a FLAIR image demonstrating high
signal in the left thalamus.
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Ve nous t hrombos is oI e in oI a le n a nd s t ra ight s inus
he n you loo clos e ly a nd you ma y ha e t o e nla rge
t he ima ge t o a ppre cia t e t his t he re is a ls o high s igna l
in t he ba s a l ga nglia on t he right .
The s e bila t e ra l Iindings s hould ra is e t he s us picion oI
de e p ce re bra l e nous t hrombos is .
s a git t a l T re cons t ruct ion de mons t ra t e s a Iilling
de Ie ct in t he s t ra ight s inus a nd t he e in oI a le n
a rrows .
n t he le It a young pa t ie nt wit h bila t e ra l a bnorma lit ie s
in t he re gion oI t he ba s a l ga nglia .
a s e d on t he ima ging Iindings t he re is a broa d
diIIe re nt ia l including s ma ll e s s e l dis e a s e
de mye linis a t ion int o ica t ion a nd me t a bolic dis orde rs .
ont inue wit h t he T1- we ight e d ima ge s in t his pa t ie nt .
ila t e ra l inIa rct ions in t he ba s a l ga nglia due t o de e p ce re bra l
e nous t hrombos is
ot ice t he a bnorma l high s igna l in t he int e rna l
ce re bra l e ins a nd s t ra ight s inus on t he T1- we ight e d
ima ge s whe re t he re s hould be a low s igna l due t o
Ilow oid.
This wa s unli e t he low s igna l in ot he r s inus e s .
The dia gnos is is bila t e ra l inIa rct ions in t he ba s a l
ga nglia due t o de e p ce re bra l e nous t hrombos is .
Venous infarction (5) - Edema
n s ome ca s e s oI e nous t hrombos is t he ima ging
Iindings ca n re s ol e comple t e ly.
n t he le It a pa t ie nt wit h a s ubcort ica l a re a oI high
s igna l int e ns it y.
The Iirs t impre s s ion wa s t ha t t his could be a low gra de
glioma .
n a Iollow up s ca n t he a bnorma lit ie s ha d re s ol e d
comple t e ly.
n re t ros pe ct a de ns e e s s e l s ign wa s s e e n in one oI
t he cort ica l e ins a nd t he dia gnos is oI e nous
t hrombos is wa s ma de .
The high s igna l int e ns it y ca n be a t t ribut e d t o
a s oge nic e de ma due t o t he high e nous pre s s ure
t ha t re s ult e d Irom t he t hrombos is .
Imaging in suspected thrombosis
CT-venography
T- e nogra phy is a s imple a nd s t ra ight Iorwa rd
t e chni ue t o de mons t ra t e e nous t hrombos is .
n t he e a rly s t a ge t he re is non- e nha nce me nt oI t he
t hrombos e d e in a nd in a la t e r s t a ge t he re is non-
e nha nce me nt oI t he t hrombus wit h s urrounding
e nha nce me nt nown a s e mpt y de lt a s ign a s
dis cus s e d be Iore .
nli e T- e nogra phy irt ua lly ha s no pit Ia lls .
The only t hing t ha t you don t wa nt t o do is t o s ca n
t oo e a rly i. e . be Iore t he e ins e nha nce or t oo la t e
i. e . whe n t he cont ra s t is gone .
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Vie w more ima ge s : 1/
ome a d oca t e t o do a s ca n li e a T- a rt e riogra phy
a nd us t a dd - 10 s e conds de la y.
To be on t he s a Ie s ide we a d oca t e 4 - 0 s e conds
de la y a It e r t he s t a rt oI cont ra s t in e ct ion.
e us e a t le a s t 0 cc oI cont ra s t .
n t he le It s ome ima ge s oI a T- e nogra phy
de mons t ra t ing t hrombos is in ma ny s inus e s .
Vie w more ima ge s : 1/ 3
n t he le It ima ge s oI a pa t ie nt wit h a n inIa rct ion in
t he a re a oI t he e in oI a bb .
n t he non- e nha nce d ima ge s you ca n a ppre cia t e t he
de ns e t hrombus wit hin t he t ra ns e rs e s inus a nd t he
he morrha ge in t he inIa rct e d a re a .
n t he e nha nce d ima ge s a Iilling de Ie ct ca n be s e e n in
t he t ra ns e rs e s inus .
ou ca n s croll t hrough t he ima ge s .
Tra ns e rs e P ima ge oI a Pha s e - ont ra s t a ngiogra phy.
The right t ra ns e rs e s inus a nd ugula r e in ha e no s igna l
due t o t hrombos is .
MR-venography
The - t e chni ue s t ha t a re us e d Ior t he dia gnos is oI
ce re bra l e nous t hrombos is a re :
Time - oI- Ilight T pha s e - cont ra s t a ngiogra phy
P a nd cont ra s t - e nha nce d - e nogra phy:
Time - oI- light a ngiogra phy is ba s e d on t he
phe nome non oI Ilow- re la t e d e nha nce me nt oI s pins
e nt e ring int o a n ima ging s lice .
s a re s ult oI be ing uns a t ura t e d t he s e s pins gi e
more s igna l t ha t s urrounding s a t ura t e d s pins .
Pha s e - cont ra s t a ngiogra phy us e s t he principle t ha t
s pins in blood t ha t is mo ing in t he s a me dire ct ion a s
a ma gne t ic Iie ld gra die nt de e lop a pha s e s hiIt t ha t is
proport iona l t o t he e locit y oI t he s pins .
This inIorma t ion ca n be us e d t o de t e rmine t he
e locit y oI t he s pins . This ima ge ca n be s ubt ra ct e d
Irom t he ima ge t ha t is a c uire d wit hout t he e locit y
e ncoding gra die nt s t o obt a in a n a ngiogra m.
ont ra s t - e nha nce d - e nogra phy us e s t he T1-
s hort e ning oI a dolinium.
t is s imila r t o cont ra s t - e nha nce d T- e nogra phy.
he n you us e P- pro e ct ions a lwa ys loo a t t he
s ource ima ge s .
n t he le It a la t e ra l a nd obli ue P ima ge Irom a
norma l cont ra s t - e nha nce d e nogra phy.
ot ice t he promine nt e in oI Trola rd re d a rrow a nd
e in oI a bbe blue a rrow .
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e ry t e chni ue s ha s it s own pit Ia lls a s we will
dis cus s in a mome nt .
ont ra s t - e nha nce d e nogra phy ha s t he
dis a d a nt a ge t ha t you ne e d t o gi e cont ra s t but ha s
le s s pit Ia lls .
DSA
ngiogra phy is only pe rIorme d in s e e re ca s e s whe n
a n int e r e nt ion is pla nne d.
n t he le It ima ge s oI a pa t ie nt wit h e nous
t hrombos is who wa s uncons ious a nd did not re s pond
t o a nt icoa gula nt t he ra py.
The re is t hrombos is oI t he s upe rior s a git t a l s inus re d
a rrow s t ra ight s inus blue a rrow a nd t ra ns e rs e a nd
s igmoid s inus ye llow a rrow .
ont inue wit h t he ide o oI t he t hrombe ct omy.
n t he le It a ide o oI t he t hrombe ct omy.
Pitfalls in CT
Arachnoid Granulations
ra chnoid gra nula t ions a re s ma ll prot rus ions oI t he
a ra chnoid t hrough t he dura ma t e r.
The y prot rude int o t he e nous s inus e s a nd ma y mimic
Iilling de Ie ct s ca us e d by t hrombus .
s ua lly t he s e gra nula t ions a re e a s ily t o diIIe re nt ia t e
Irom t hrombos is .
Pseudodelta sign
The de ns e t ria ngle s ign ca n be mimic e d in inIa nt s by
t he combina t ion oI t he hypoint e ns it y oI t he
unmye lina t e d bra in a nd t he phys iologic polycyt he mia
re s ult ig in high de ns it y oI t he blood in t he s a git t a l
s inus .
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Ps e udode lt a s ign in a n inIa nt
ps e udode lt a s ign ca n a ls o be s e e n in pa t ie nt s wit h
hype ra t t e nua t ing a cut e s uba ra chnoid he morrha ge
a round t he s inus or s ubdura l e mpye ma or in pa t ie nt s
wit h a pos t e rior pa ra Ia lcine int e rhe mis phe ric
he ma t oma .
n t he s e ca s e s a dminis t ra t ion oI cont ra s t ma t e ria l
s hould opa ciIy t he s inus oblit e ra t ing t he luce nt ce nt e r
oI t he ps e udode lt a .
orma l t ra ns e rs e s inus le It a nd t hrombos e d t ra ns e rs e
s inus right .
orma lly e ins a re s light ly de ns e r t ha n bra in t is s ue
a nd in s ome ca s e s it is diIIicult t o s a y whe t he r it is
norma l or t oo de ns e .
n t he s e ca s e s a cont ra s t e nha nce d s ca n is ne ce s s a ry
t o s ol e t his proble m.
n t he le It a n ima ge oI a t hrombos e d t ra ns e rs e s inus
a nd ne t t o it a norma l t ra ns e rs e s inus .
Wrong bolus timing
n t he le It t hre e ima ge s oI a pa t ie nt wit h e nous
t hrombos is in t he s upe rior s a git t a l s inus .
n t he Ia r le It we s e e a de ns e e s s e l s ign on t he
une nha nce d T.
n t he middle a n ima ge ma de 2 s e conds a It e r t he
s t a rt oI t he cont ra s t in e ct ion.
The re is a rt e ria l e nha nce me nt a nd it loo s a s iI t he
s upe rior s a git t a l s inus e nha nce s but in Ia ct wha t we
s e e is t he s hine t hrough oI t he de ns e t hrombus .
nly on t he ima ge on t he right which wa s ma de 4
s e conds a It e r cont ra s t in e ct ion t he re is a n e mpt y
de lt a s ign which pro e s t he pre s e nce oI a t hrombus
in t he s inus .
Hematoma simulating venous thrombosis
s ua lly t he re is no proble m in diIIe re nt ia t ing a
he ma t oma Irom a t hrombos e d s inus .
n t he le It a pa t ie nt wit h a pe riphe ra l int ra ce re bra l
he ma t oma t ha t on Iirs t impre s s ion s imula t e s a
t hrombos e d t ra ns e rs e s inus .
n t he le It a pa t ie nt wit h a n s ubdura l he ma t oma t ha t
in t he re gion oI t he s upe rior s a git t a l s inus re s ult s in a
ps e udo e mpt y de lt a s ign.
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y s crolling t hrough t he da t a s e t it wa s ob ious t ha t
it wa s a n e t e nt ion oI t he he ma t oma .
Pitfalls in MRI
Hypoplastic transverse sinus
ypopla s ia a nd a pla s ia oI t he right or le It t ra ns e rs e
s inus is a common Iinding.
t ca n e a s ily be mis t a e n Ior s inus t hrombos is
be ca us e on t he one oI t he t ra ns e rs e s inus e s is
mis s ing.
he n you s us pe ct t ha t t he re is a hypopla s t ic
t ra ns e rs e s inus t he n you s hould loo a t t he s i e oI
t he ugula r Iora me n.
n t he le It ima ge s oI a pa t ie nt wit h hypopla s ia oI t he
le It t ra ns e rs e s inus .
ot ice t he s i e diIIe re nce oI t he ugula r Iora me n.
n t he le It a t ra ns e rs e P oI pha s e - cont ra s t
ima ge s .
To diIIe re nt ia t e whe t he r t he re is a hypopla s t ic
t ra ns e rs e s inus or t hrombos e d s inus you ne e d t o
loo a t t he s ource ima ge s .
n t he s ource ima ge on t he right you ca n s e e t ha t
t he re is no hypopla s ia blue a rrow .
n t his ca s e t he re t hrombos is oI t he le It t ra ns e rs e
s inus .
n t he le It a not he r ca s e t ha t de mons t ra t e s t ha t you
ca nnot Iully re ly on pha s e cont ra s t ima ging.
The s igna l in t he e in de pe nds on t he e locit y oI t he
Ilowing blood a nd t he e locit y e ncoding by t he
t e chnicia n.
n t he Ia r le It a pa t ie nt wit h non is ua li a t ion oI t he
le It t ra ns e rs e s inus .
This could be hypopla s ia e nous t hrombos is or s low
flow.
n t he cont ra s t e nha nce d T1- we ight e d ima ge it is
ob ious t ha t t he s inus Iills wit h cont ra s t a nd is pa t e nt .
Low signal intensity in thrombus
orma lly whe n t he re is low s igna l in a e in it is
a t t ribut e d t o Ilow oid a nd a s ign oI pa t e ncy oI t he
e in.
owe e r a t s ome s t a ge oI t he t hrombus t he re is
int ra ce llula r de o yhe moglobin which is da r on T2
a nd mimics Ilow oid.
n t he le It t he re is a t hrombos e d right t ra ns e rs e
s inus wit h a de lt a s ign on t he cont ra s t e nha nce d
ima ge .
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Thrombus in right transverse sinus is dark on T2 due to
intracellular deoxyhemoglobin (Courtesy dr. Howard Rowley)
The sinus has a low signal intensity on the T2-
weighted image as a result of the intracellular
deoxyhemoglobin.
On the contrast enhanced T1-weighted image it is
obvious that the sinus is filled with thrombus.
Flow void on contrast-enhanced MR
On the contrast enhanced T1 images on the left there
is an area of low signal intensity within the enhancing
transverse sinus.
This could easily been mistaken for a central thrombus
within the sinus.
This however is the result of flow void.
Continue with the phase contrast images.
On the phase contrast images it is obvious that the
transverse sinus is patent.
We can conclude that MRI has many false positives
and negatives in the diagnosis of venous thrombosis.
Contrast enhanced MR-venography is the most
reliable MR technique. CT-venography is even more
reliable, because it is easy and less sensitive to
pitfalls.
Pitfalls in TOF imaging are:
Signal loss due to in-plane flow.
Flow simulated by T1-shine thru of methemoglobin
within thrombus.
Chronic dural sinus thrombosis and
related syndromes
DAVF
Chronic dural sinus thrombosis can lead to dural
arteriovenous fistula formation and to increased CSF
pressure.
A DAVF or dural arteriovenous fistula is an abnormal
connection between dural arteries, which are branches
of the external carotid with the venous sinuses. Sinus
thrombosis is seen in many patients with a dural
arteriovenous fistula, but the pathogenesis is still
unclear (10).
There are two possible mechanisms: (a)
thrombophlebitis of the dural sinus may induce a dural
fistula and (b) in the course of a dural fistula flow
reversal may lead to thrombosis.
Current classifications of DAVF focus mainly on the
presence of leptomeningeal reflux related to cerebral
venous hypertension leading to cerebral venous
infarction or hemorrhage.
On the left DSA images of a patient with a DAVF.
Notice the direct communication between the
branches of the external carotid artery and the
transverse sinus (blue arrow).
Continue with the T2-weighted images.
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On the left T2-images during the follow up.
In april 2008 there were no abnormalities.
In january 2009 there are signs of intracranial
hypertension like CSF surrounding the optic nerve and
CSF within the stalk of the hypophysis.
Thrombosis and increased CSF pressure
In some patients dural sinus thrombosis may, even
after recanalisation, lead to persisting disturbances in
venous circulation.
This may lead to raised intracranial CSF pressure as
assessed by lumbar puncture.
Clinically, these patients complain of headaches and
they may have vision disturbances due to papil
edema.
On MRI, one may see increased CSF around the optic
nerve and an empty sella.
Apparently in some patients a residual stenosis
persists.
On the left a T2-weighted image demonstrating papil
edema and an empty sella.
Continue with the sagittal T1-weighted image.
On the left a sagittal T1-weighted image
demonstrating the empty sella (arrow).
Venous territories
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On the left an illustration of the territories of the
venous drainage.
There is great variation in these territories and the
illustration should be regarded as a rough guide.
References
1. Imaging of Cerebral Venous Thrombosis: Current Techniques, Spectrum of Findings, and Diagnostic Pitfalls
by James L. Leach et al
October 2006 RadioGraphics, 26, S19-S41
2. Brain, Venous Sinus Thrombosis
in eMedicine by Mahesh R Patel
3. Diagnostic Value of Multidetector-Row CT Angiography in the Evaluation of Thrombosis of the Cerebral Venous
Sinuses
by J. Linn et al
American Journal of Neuroradiology 28:946-952, May 2007
4. Cerebral Venous Thrombosis and Multidetector CT Angiography: Tips and Tricks
by Mathieu H. Rodallec et al
October 2006 RadioGraphics, 26, S5-S18.
5. The Empty Delta Sign
by Emil J. Y. Lee
September 2002 Radiology, 224, 788-789.
6. Radiologic Diagnosis of Cerebral Venous Thrombosis: Pictorial Review
by Colin S. Poon et al
AJR 2007; 189:S64-S75
7. PDF: Cerebral venous thrombosis: pathogenesis, presentation and prognosis
by J van Gijn
JRSM Volume 93, Number 5 Pp. 230-233
8. Superior Sagittal Sinus Thrombosis: Subtle Signs on Neuroimaging
by Phua Hwee Tang et al
Ann Acad Med Singapore 2008;37:397-401
9. Comparison of CT Venography with MR Venography in Cerebral Sinovenous Thrombosis
by N. Khandelwal et al
AJR 2006; 187:1637-1643
10. Intracranial dural arteriovenous fistulas with or without cerebral sinus thrombosis: analysis of 69 patients
by L K Tsai et al
J Neurol Neurosurg Psychiatry 2004;75:1639-1641
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