REVIEW ARTICLE
Cerebral Venous Thrombosis
C Prakash*, BC Bansal**
The syndrome of intracranial venous and sinus
thrombosis - termed as cerebral venous thrombosis
(CVT) was recognised in early part of 18th century
when Ribes1 (1825) described, in a 45 yrs old man
suffering from disseminated malignancy, the clinical
and autopsy spectrum of superior sagittal sinus
thrombosis. The first ever description of superior
sagittal sinus thrombosis occurring in puerperium was
by Abercrombie in 1828 2 . Kalabagh in his
monograph on CVT stated that aseptic thrombosis is
not an uncommon entity especially in children,
puerperium, and elderly3. With the advent of three
dimensional M.R. Flow Imaging it has been shown
that the prevalence of CVT is more common than
reported previously and carries a less serious
prognosis4.
Exact incidence of CVT is still under debate because
of scarcity of scientifically planned epidemiological
studies in the available literature. Hospital data has
been utilised to determine its prevalence in the
community. According to British Registrar General5,
average mortality from CVT in U.K. during 1952-
1961, was 0.4/106/per year. On assumption that
mortality rate from CVT is 10%, it’s prevalence in U.K.
is likely to be 4.0/106/per yr. On the other hand
aseptic CVT occurring in pregnancy and puerperium
has been reported very frequently from Indian
subcontinent. While studying stroke in the young,
Indian studies6,7,8 revealed that CVT constitutes 10-
15% of stroke in the young and was the commonest
cause of stroke in pre-menopausal women.
Sirinivasan7 encountered 50 cases of severe CVT
amongst 1000 deliveries performed per year. It has
been estimated that the prevalence rate in developing
countries is approximately 10 times more than that
in developed countries. In pre-antibiotic era, post-
infective CVT was more prevalent while in post-
antibiotic era, aseptic CVT has taken its place.
* Former Director and Head of Department of
Medicine, Rohtak Medical College, Rohtak,
Haryana.
** Professor of Medicine and Head of Neurology
Division (Retd.), Rohtak Medical College, Rohtak;
Senior Consultant in Neurology, Moolchand K.R.
Hospital, New Delhi.
Scanning age-related incidence graphs9,10 reveal
three peaks that are as follows:
1. Infants and young children : Probably explained
on the basis of greater prevalence of dehydration-
associated disease, malnutrition (marasmus) and
infections of central nervous systems e.g., pyogenic
meningitis, etc.
2. Young Premenopausal Women : Frequent use
of oral contraceptives in developed countries is
an important aetiologic factor; while in developing
countries, pregnancy and puerperium are the
common causes.
3. Elderly : Greater prevalence of malignancies,
malnutrition and dehydration-associated disorders
explain the frequency of CVT in elderly.
Applied Anatomy 12,13
Cerebral venous circulation exhibits following
anatomical characteristics that influence clinical profile
and management of CVT :
a) Cerebral veins and sinuses have neither any valves
nor tunica muscularis. Absence of valves permits
blood flow in various directions while absence of
tunica muscularis permits veins to remain dilated.
b) Intercommunication between various venous
sinuses either via communicating veins (vein of
Trolard, & Vein of Labbe) or through merger into
each other especially at torcular Herophili,
explains lack of correlation between the severity
of underlying pathology and infrequent clinical
symptomatology. Even recovery that is complete
or with minimal sequelae, is explained by this fact.
c) Venous sinuses are located between two rigid
layers of duramater. This prevents their
compression when intracranial pressure rises.
d) Emissary veins from scalp, face, paranasal sinuses
and ears, etc., diploic veins, and meningeal veins
drain into cerebral venous sinuses either directly
or via venous lacunae. This explains the frequent
occurrence of CVT as a complication of infective
pathologies in the catchment areas, e.g.,
cavernous sinus thrombosis in the facial infections,
 lateral sinus thrombosis in chronic otitis media
and sagittal sinus thrombosis in scalp infections.
e) Superficial cortical veins drain into superior sagittal
sinus against the blood flow in the sinus, thus
causing turbulation in the blood stream that is
further aggravated by the presence of fibrous
septa present at inferior angle of the sinus. This
fact explains greater prevalence of superior
sagittal thrombosis.
f) Arachnoid villi are located in the walls of superior
sagittal sinus and drain CSF into the sinus. So,
thrombosis when it develops in the sinus, especially
in the posterior segment, blocks villi and leads to
intracranial hypertension and papilloedema.
g) Deep cortical veins, like arterial circle of Willis,
also form a venous circle around mid-brain,
comprising of basal vein of Rosenthal formed by
the merger of anterior and middle cerebral veins,
formed by the drain into internal cerebral vein
posteriorly that merges into the vein of Galen.
These basal veins become engorged in superior
sagittal sinus thrombosis and can be
demonstrated by venous transcranial doppler
ultrasonography in 80% cases14.
h) Cerebral venous system can be classified into two
major groups:
1. Superficial system comprising sagittal sinuses
and cortical veins draining superficial surfaces
of both cerebral hemispheres.
2. Deep system comprises lateral sinus, straight
sinus, and sigmoid sinus alongwith draining
deeper cortical veins.
i) Superior sagittal sinus is the commonest sinus to
be involved in aseptic CVT (Table I)3.
Table I : Showing frequency of various sinuses
involved in aseptic CVT
Superior sagittal sinus 72%
Lateral sinus (combined) 70%
Straight sinus 13%
Aetiology
CVT like venous thrombosis at other sites in the body,
can develop because of :
a) Changes in the vessel walls (phlebitis or
phlebopathy) e.g., malignant infiltration, post-
infective phlebitis, etc.
56
b) Changes in blood flow, e.g., stasis or
hyperviscosity of blood as in dehydration, C.H.F.,
polycythaemia.
c) Changes in coagulability of blood, e.g.,
thrombocythaemia, protein S & C alterations,
Antithrombin deficiency, antiphospholipid
antibodies, etc.
In view of the above, many pathological conditions
which are associated with CVT, have been described.
More commoner ones are shown in the Table II.
Table II : Aetiologic Causes of CVT
a) Hypercoagulable Conditions.
Pregnancy & Puerperium
Oral Contraceptives15
Anti-thrombin III deficiency16
Antiphospholipid Syndrome16
Protein C & S alterations16
Factor V Leiden and factor II gene mutations17
b) Changes in vessel wall.
Malignancy
Infections : local-chronic-otitis media, nasolabial and/or
facial infections, pyogenic meningitis
– Systemic, e.g., gram negative septicaemia, fungal infections
etc.
c) Changes in blood flow/viscosity.
Marasmus
Malnutrition
Dehydration
Congestive heart failure
Hyperviscosity syndrome
A. Post-infective CVT18,19,19A
In pre-antibiotic era, pyogenic infections in the
catchment area were the commonest cause of
CVT. Infective organism reaches the draining sinus
via emissary veins. Though any sinus can be
involved, still, commonly involved in order of
frequency, are cavernous sinus, lateral sinus and
superior sagittal sinus. With the advent of
antibiotics, incidence of post-infective CVT has
markedly reduced but still otitic hydrocephalus as
a result of lateral sinus thrombosis is a common
sequelae of chronic suppurative otitis media.
B. CVT in Premenopausal Women19,20,21,25
a. Post-gestational & post-puerperal CVT. This
entity though prevalent globally, has been
described more often from Indian
Journal of Indian Academy of Clinical Medicine
Vol. 5
No. 1
 subcontinent-post-puerperal is more common
than post-gestational. In the latter, it occurs
only in the last trimester especially in the last
week. Underlying pathogenic factor in
pregnancy and puerperium is
hypercoagulibility that occurs due to following
alterations15:
i) Increased level of fibrinogen, factor VII,
VIII, and X.
ii) Diminution in inhibitors of coagulant
proteins S, in pregnancy and puerperium.
iii) Rise in inhibitors of protein C level.
iv) Ability to neutralize heparin has been
shown to rise during pregnancy.
v) Factor V Leiden and Factor II gene
mutation17 which has been extensively
studied and proved to be an important
predisposing factor in post-oral
contraceptive. Role of these factors have
not been studied in post-puerperial CVT.
Earlier observations regarding aetiologic role of
stasis, puerperial sepsis and paradoxical venous
embolism via vertebral plexus, have not been
proved by scientific studies.
Various biochemical alterations that play role in
the aetiology of arterial atherosclerotic disease
have also been studied in post-puerperal CVT. It
has been observed that serum triglycerides,
phospholipids and free fatty acids show mild rise
while fibrinolytic activity diminishes23,24. Platelet
count and adhesiveness also show an increase22.
Statistical correlation studies disproved their role
in aetiopathogenesis of CVT.
Reasons for its frequent occurrence in
socioeconomically backward persons especially
of Indian origin need to be researched.
b) Post-oral contraceptive CVT
Use of oral contraceptives has been identified
as an important cause of CVT in developed
countries. Prolonged use of oral contraceptives
leads to acquired “activated protein C
resistance”. This phenomenon gets
aggravated if factor V Leiden and factor II gene
mutations are present; increasing the risk of
thrombosis by 10 times. This fact provoked
Vandenbroucke to postulate a mandatory pre-
prescription testing of the potential user of oral
Journal of Indian Academy of Clinical Medicine
Vol. 5
contraceptive.
c) Malignancy Associated CVT
CVT is commonly associated with advanced
malignancy. Thrombotic propensity may
accelerate due to infiltration of vessel walls,
and/or generation of abnormal coagulant
factors. CVT as a paraneoplastic manifestation
also has been described28.
Pathology29
Pathological findings observed in central nervous
system as a result of CVT are determined by a)
underlying disease pathology; b) nature of sinus/
cerebral vein involved; c) interval between the onset
and pathological examination.
Cortical vein thrombosis usually presents as a cord
like swelling with minimal or absent haemorrhagic
infarction of the brain. This discrepancy has been
explained on the presence of frequent
intercommunications between various cortical veins
and sinuses.
In case of superior sagittal sinus thrombosis, sinus is
distended and appears blue. Cortical veins are also
swollen and may rupture at some places giving rise
to haemorhagic infarction and even intercerebral
haemorrhage. In an occasional case, haemorrhagic
infarction may appear on the other side due to
occlusion of opposite cortical vein (parasagittal). In
deep cerebral vein thrombosis, white matter may be
involved, eg., basal ganglia, thalamus, etc. As time
passes, thrombosis gets recanalised, organized and
may even disappear in majority of cases.
Cerebral edema with or without increased intracranial
hypertension is a frequent finding in early stage. It
may even lead to transtentorial herniation with
notching of uncus of temporal lobe.
Microscopy shows typical changes of haemorrhage,
but specific feature appears to be “profuse leukocytic
invasion” because of patent arteries allowing inflow
of inflammatory cells.
Clinical Picture
Clinical profile is determined by a) underlying sinus/
venous system involved; b) mode of onset, i.e., acute,
subacute or chronic; c) time interval between onset
of disease and clinical presentation; d) nature of

No. 1 57
primary disease giving rise to CVT.
As stated earlier, CVT is an uncommon condition in
developed countries and hence unless this condition
is suspected prior to embarking on investigations, the
diagnosis is likely to be missed. Therefore it is
reasonable to entertain this diagnostic possibility if
the circumstances are conducive to development of
CVT. Presence of deep vein thrombosis (calf, crural
or pelvic) or pulmonary embolism may be an
important pointer to the occurrence of CVT25.
In Indian subcontinent, post-puerperal CVT being the
commonest, clinical picture usually comprises a young
premenopausal female, who 7-10 days after normal
delivery, presents with severe headache, low grade
fever, unifocal or multifocal seizures and neurologic
deficit of various magnitude and severity. As arachnoid
villi are likely to get blocked due to thrombus
developing specially in the posterior segment,
papilloedema occurs in 40% cases. Sometimes patient
may present with severe headache and papilloedema
without any neurologic deficit simulating a brain
tumour – pseudotumour cerebri27.
Focal neurological deficit comprises hemiparesis
usually with facial sparing (as “face area” in cerebral
cortex is drained by sylvian vein which is a tributary
of cavernous sinus) and lower limb more severely
affected than upper limb 13,25 . In some cases,
contralateral cortical veins may be involved resulting
in paresis or paralysis of the opposite lower limb thus
giving rise to paraparesis or paraplegia30,31. Cortical
deficits like aphasia, agnosia, apraxia, and cortical
blindness are not uncommon but are fleeting in
nature.
Seizures – unifocal or multifocal, are present in 50%
cases33. They may be localized at the onset but may
later become generalized. Rarely they may persist
after an acute phase is over. Their early appearance
is the hallmark of bad prognosis. Kinetic autism of
short duration manifesting during recovery phase,
have been reported. E.E.G. shows intermittent delta
activity in frontal area.
The preceding discussion relates predominately to
superior sagittal sinus or its superficial tributaries.
Clinical profile of patients in whom deeper cerebral
veins and/or draining sinuses are involved is complex.
It may comprise hyperpyrexia, varying degree of loss
of consciousness, fluctuating blood pressure, and
massive quadriplegia. Cranial nerves may be involved
58
if midbrain and/or pons is affected. Prognosis is not
good though a few recoveries have been reported.
Deep veins/sinuses thrombosis is rarer and affects
commonly children though a few cases in pre-
menopausal females have been reported.
Rarely concomitant arterial involvement in association
with CVT complicates the clinical profile and must be
kept in mind when confronted with a complex clinical
picture.
Intracranial venous thrombosis may be so insidious
that it is only detected on post-mortem examination
particularly in elderly patients dying of congestive
cardiac failure31.
Cavernous sinus thrombosis 19
As it is usually post-infective, its incidence has
markedly diminished after the advent of antibiotics.
Recently there has been a spurt in the incidence of
cavernous sinus thrombosis due to emergence of drug
resistant organisms and greater prevalence of
immuno-suppressive disorders. Sources of pyogenic
organisms are nasolabial territory and paranasal
sinuses.
Clinical picture comprises high fever with chills or
rigors, orbital or retro-orbital pain, chemosis,
proptosis, orbital congestion, and oculomotor
disturbances due to involvement of oculomotor,
trochlear, and abducent nerves. Ocular oedema and/
or compression of optic nerve may result in blindness.
Inter-cavernous internal carotid artery may be involved
leading to hemiparesis, etc. Early institution of
antibiotics is mandatory for minimising sequelae.
Lateral sinus thrombosis3
Thrombosis of lateral sinus or its tributaries is mostly
secondary to infections of middle ear or mastoid
region. Hence, advent of antibiotics should have
reduced the incidence of this entity but due to
unknown reasons, otitic hydrocephalus secondary to
latera sinus or transverse sinus thrombosis following
C.S.O.M. and chronic mastoiditis is still not an
uncommon entity.
Investigations
Objectives of investigations are a) diagnosis of
cerebral vein/sinus thrombosis; b) identification of vein
or sinus involved; c) identification of underlying
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Vol. 5
No. 1
pathogenic factors; d) evaluation of C.N.S. damage.
The following investigations are at present in vogue :
a. Cerebral Angiography: It is an invasive
technique and delayed films are essential, as
cerebral venous system is visualized in delayed
films due to slow and stagnant circulation.
Angiography is neither sensitive nor very specific.
Digital intravenous angiography provides better
visualisation of dural venous sinuses. As cerebral
veins are not visualised as well as dural sinuses, it
has not gained popularity34.
b. Radionuclide Scanning35: Dynamic radionuclide
scanning has been utilized for visualization of
various dural sinuses but because of lack of
specificity, it has entered the antique list.
c. C.T. Scan 36,37: During CT Scan, both non-
enhanced and enhanced films are required.
Various abnormalities on C.T. Scan are as follows:
i) Dense triangle sign because of thrombosis in
the sinus. Quantitative measurement of
attenuation or density may help to differentiate
between clotted blood and non-clotted blood.
ii) Cerebral oedema (localised/generalized).
iii) Haemorrhagic infarction and inter-cerebral
hemorrhages.
iv) Cord sign – an irregular and high density
lesion located in the superficial aspect of the
cerebral hemispheres. It represents
thrombosed cortical vein.
v) Delta sign or empty triangle sign. It is
demonstrated on enhanced CT as a filling
defect in the posterior part of superior sagittal
sinus thrombosis.
d. Magnetic Resonance Imaging 38 : Since the
advent of three dimensional MR Flow Imaging,
non-invasive diagnosis of thrombosis in various
stages of development has been made possible.
Routine use is likely to throw more light on its
prevalence, aetiologic risk factors, course of
disease and efficacy of treatment instituted. MR
angiography not only seems to offer an important
advantage as a non-invasive tool in diagnostic
procedures but also seems useful as a follow-up
instrument for documentation of thrombus
regression, recanalisation and venous
collateralisation. Cost and logistic problems
especially when patient is in intensive care unit
Journal of Indian Academy of Clinical Medicine
Vol. 5
are the main limiting factors.
Usual findings on MRI are isointense signal in TI
and hyperintense signal in T2 on Ist to 5th day
and signal becomes hyper-intense in both T I & II
on 5th to 15th days.
e. Venous Transcranial Doppler Ultrasound 14:
Has recently been used for identification of
engorged basal vein of Rosenthal which becomes
distended, tortuous and prominent in superior
sagittal sinus thrombosis. This is a noninvasisve
investigation and is indicated to monitor the
progress of the disease. Specificity is only 80%
and it provides an indirect evidence.
f. Miscellaneous: CSF examination may reveal
non-specific changes, e.g., increased pressure,
increased proteins and pleocytosis, RBC may be
seen in large numbers and even in clumps. EEG
may show hyperactivity, which is lateralised. These
changes are more prominent in post-infective CVT.
Treatment
As the patient’s consciousness is impaired and
underlying neuropathology is still progressing, he is
to be admitted in intensive care unit and needs
treatment accordingly. Specific measures include
institution of nursing care, prevention of pressure sores
and urinary tract infection, anti-cerebral oedema
therapy and anti convulsant therapy for seizures. A
close watch for dehydration secondary to excessive
use of diuretics and other anti-cerebral oedema
measures is essential as the resultant
haemoconcentration increases thrombotic tendency.
Use of heparin in CVT has been debated for a long
time. In the past, main arguments cited against its
use were the presence of haemorrahgic infarction,
inter-cerebral haematoma and sub-arachnoid
hemorrhage. Scientifically planned studies had
generated enough evidence in favour of heparin use
and thus it has emerged as a useful drug in the
management of CVT39,40,41,42. Heparin reduces both
mortality and morbidity in CVT. Low molecular weight
heparin has also been found to be equally effective.
Heparin counteracts the thrombotic action of
thromboplastins released by infarcted brain tissue.
Encouraged by success of institution of heparin
therapy, thrombolytic and fibrinolytic drugs like
urokinase, streptokinase and oral anticoagulants,
e.g., warfarin have also been tried and found to be

No. 1 59
effective in some cases43,44. As it is difficult to draw
conclusions on the basis of anecdotal data presently
used in available studies, more work is needed to
evaluate their efficacy.
Surgical decompressive craniotomy, thrombectomy
and evacuation of inter-cerebral haematoma need
still further evaluation before it is recommended as a
safe procedure6,45.
Prognosis
Early clinical diagnosis, three dimensional MR flow
imaging studies, and early institution of therapy
specially heparin or thrombolytic therapy followed by
oral anticoagulants have improved the prognosis of
CVT. Srinivasan observed that mortality has been
reduced from 50.6% to 10% in the last three
decades10.
Factors adversely affecting prognosis are early
appearance of the convulso-paralytic state,
impairment of consciousness, and presence of
haemorrhagic infarcts demonstrated by CT or MRI.
Usually recovery is either complete or associated with
minimal neurological deficit because of recanalisation
and dissolution of thrombosis. The risk of future
recurrence appears to be very infrequent, rather
unknown.
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