7/25/2019 jact00i1p55

1/7

R E V I E W A R T I C L E

* 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.

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 18282. Kalabagh in his

monograph on CVT stated that aseptic thrombosis isnot 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%, its 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 studies6,7,8revealed 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 CVTamongst 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.

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 isan 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 Anatomy12,13

Cerebral venous circulation exhibits following

anatomical characteristics that influence clinical profileand 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 clinicalsymptomatology. 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 infectivepathologies in the catchment areas, e.g.,

cavernous sinus thrombosis in the facial infections,

7/25/2019 jact00i1p55

2/7

56 Journal of Indian Academy of Clinical Medicine Vol. 5 No. 1

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 fibroussepta 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 sinusesand 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.

b) Changes in blood flow, e.g., stasis or

hyperviscosity of blood as in dehydration, C.H.F.,

polycythaemia.

c) Changes in coagulabil ity of blood, e.g.,

thrombocythaemia, protein S & C alterations,

An ti thrombin defic iency, an tiphospho lipidantibodies, 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

DehydrationCongestive 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 ofantibiotics, 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

7/25/2019 jact00i1p55

3/7

Journal of Indian Academy of Clinical Medicine Vol. 5 No. 1 57

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

mutation17which has been extensively

studied and proved to be an importantpredisposing 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. Ithas 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 CVTUse 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

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 cordlike 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, haemorrhagicinfarction 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

7/25/2019 jact00i1p55

4/7

58 Journal of Indian Academy of Clinical Medicine Vol. 5 No. 1

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 ifthe 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 thrombusdeveloping 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 limb13,25. In some cases,

contralateral cortical veins may be involved resultingin 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

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 associationwith 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 thrombosis19

As it is usually post-infective, its incidence hasmarkedly 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 tounknown 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

7/25/2019 jact00i1p55

5/7

Journal of Indian Academy of Clinical Medicine Vol. 5 No. 1 59

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. Scan36,37

: 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 densitylesion 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 Imaging38: 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

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 Ultrasound14: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 patients 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 oedematherapy 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 useand 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

7/25/2019 jact00i1p55

6/7

60 Journal of Indian Academy of Clinical Medicine Vol. 5 No. 1

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 needstill 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.

References1. Ribes MF. Des recherches faites sur la phlebite Revue Medical

Francais et Etrangere er Journal de clinique del Hotel Dieu

et de la Charite de Paris 1825; 3: 5 (cited in 24).

2. Aberombei J. Superior sagittal thrombosis in puerperium 83.

In Pathological and Practical Researches of the Brain and

Spinal CordPubl. John Carfare and Sons Edinburgh 1828;

(cited in 15).

3. Kalbag RM, Wolf AL. Etiology of cerebral venous thrombosis

in Cerebral Venous Thrombosispubl. Ed Kalbagh RM, Wolf

AL. Oxford University Press London1967; pp238.

4. Bianchi D, Maeder P, Bogousslavesky J, et al. Diagnosis of

cerebral venous thrombosis with routine magnetic resonance,an update. Eur Neurol1998; 40 (4): 79-90

5. De Bruijin SF, Stam J, Koopman MM, Vandenbroucke JP. Case

control study of risk of cerebral sinus thrombosis in oral

contraceptive users and in carriers of hereditary

prothrombotic condition. The Cerebral Venous Sinus

Thrombosis Study Group. BMJ1998; 316: 589-92.

6. Nagaraja D, Tally AB. Stroke in the young in progress in

Clinical NeurosciencesEdt publ Sinha KK, Ranchi 1988; 2:

129-45.

7. Chopra JS, Prabhakar S. Clinical features and risk factors in

stroke in young.Acta Neurologica Scandivia1979; 43: 289-300.

8. Abraham J, Shetty C, Joss C. Stroke in the young. Stroke

1971; 2: 258-66.

9. Srinivasan K. Stroke in the young. Neurology India1988;

36: 189-94.

10. Srinivasan K. Cerebral venous and arterial thrombosis in

pregnancy and puerperium.Angiology1983; 134: 737-46.

11. Carroll JD, Leak D, Lee HA. Cerebral venous thrombosis inpregnancy and puerperium. Quar J Med 1966; 35: 347-

50.

12. Barnett HJM, Hyland HH. Noninfective intracranial venous

thrombosis. Brain1953; 76: 36-45.

13. Wilterdink L, Easton JD. Cerebral ischemia in Neurologyi.e. complications of pregnancy Ed: Davinsky O, Feldmann

E, Hainline B. Publ Raven Press NY1994; 1-23.

14. Valudera JM, Schultz M, Harms L, Einhaupl KM. Venous

transcranial doppler ultrasound, monitoring in acute dural

sinus thrombosis. Stroke1995; 26 (1): 1196-9.

15. Matinelli I, Sacchi E, Landi G, et al. High risk of cerebral

venous thrombosis in carriers of prothrombotic gene mutation

and in users of oral contraceptives.N Eng J Med1988; 338:1793-7.

16. Huges CRV. The antiphospholipid syndrome. Lancet1993;

342: 341-4.

17. Vandenbroucke J. Cerebral sinus thrombosis and oral

contraceptive (editorial). BMJ1998; 317: 878-9.

18. Murthy JMK, Chopra JS, Malik SRet al. Clinico-pathological

correlates in autopsy in pyogenic meningitis. Ind J Med Res

1983; 78: 234-52.

19. Mathew NT, Meyers JS, Taori CM et al. Internal carotid artery

thrombosis in cavernous sinus thrombosis.Arch Neuro1971;

24: 11-5.

19a. Bouser MG, Chiras J, Sauron B, Castaigra P. Cerebral venousthrombosis-review of 38 cases. Stroke1985; 16: 199-213.

20. Srinivasan K. Puerperal cerebral venous thrombosisSeminar

in Neurology1988; 8: 222-5.

21. Dalal PM. Stroke in India. Jap Heart Jour1982; 46: 621-5.

22. Prakash C, Arya RK, Singla KP et al. Platelet adhesiveness

and serum lipids in cerebral venous thrombosis. J Ass PhyInd 1970; 18: 816-9.

23. Bansal BC, Prakash C, Gupta RR et al. Study of serum lipids

and fibrinolytic activity in cerebral venous thrombosis during

puerperium.Am J Obst Gyn1974; 119 (8): 1079-82.

24. Bansal BC, Prakash C. Serum lipids, platelet and fibrinolytic

activity in cerebrovascular disease. Stroke1978; 9: 137-9.

25. Daif A, Awada A, Al-Rajeh et al. Malibary Cerebral venous

thrombosis in adults a study of 40 cases from Saudi Arabia.

Stroke1995; 26: 1193-5.

26. Bansal BC, Gupta RR, Prakash C. Stroke during pregnancyand puerperium. Jap Heart J1980; 21 (2): 171-83.

27. Valerie AP, Jonathan D, Trobe MD, Kosmorks G.

Neuroophthalmic features of cerebral venous obstruction.

Arch Neuro1966; 3 (4): 280-3.

28. Ellie E, Beouran Y, Brunet R. Paraneoplastic cerebral venousthrombosis. France Review Neurology1993; 149: 297-9.

29. Banerjee AK, Chopra JS, Sawhney BB. Puerperal cerebral

venous thrombosis. Study of autopsy material. Neurology

7/25/2019 jact00i1p55

7/7

Journal of Indian Academy of Clinical Medicine Vol. 5 No. 1 61

India 1973; 21: 19-22.

30. Prakash C, Singh S. Cerebral venous thrombosis in

puerperium. J Ass Phys India1960; 8: 363-5.

31. Janaki S, Thomas L. Neurological complications in pregnancy

and puerperium. Neurology India1963; 11: 128-30.

32. Crawford SC, Digrek B, Parmer CA. Thrombosis of deep

veins of brain in adults. Arch Neuro1995; 52 (11): 1101-08.

33. Srinivasan K, Ramamurti B. Neurological disorder in

pregnancy and puerperium. J Ass Phy India1971; 19: 705-

07.

34. Barnes BD, Brant-Zawadzki M, Mentzer W. Digital substractionangiography in the diagnosis of superior sagittal sinus

thrombosis. Neurology1983; 39: 508.

35. Barnes BD, Winestock DP. Dynamic radionuclide scanning

in the diagnosis of thrombosis of superior sagittal sinus.

Neurology1977; 27: 656.

36. Brant-Zawadzki M, Chang ZY, Mccarty GE. Computed

tomography in dural sinus thrombosis. Arch Neuro1982;

39: 446-9.37. Maheshwari MC, Bhargave S. Evaluation of peripartum stroke

by C.T. Scan. Clinical Radiology1983; 34: 633-7.

38. Dormont D, Axionnat R et al. MRI in cerebral venous

thrombosis. J Neuroradiology1994; 21 (2): 81-99.

39. Einhaupl EM, Villringer A et al. Heparin in cerebral venous

thrombosis. Lancet1991; 338: 597-600.

40. Dirocco C, Lannelli A, Leonac G et al. Heparin-urokinase

treatment in aseptic dural sinus thrombosis.Arch Neuro1981;

38: 431-5.

41. Cepri S, Gangeni A, Campolo C et al. High dose heparin

plus warfarin administration in non traumatic dural sinus

thrombosis-a clinical and neuroradiological study. J

Neurosurgical Scie1998; 42 (1): 23-32.

42. Nagaraja D, Tally AB, Haridas VT et al. Heparin in

haemorrhagic infarction in cerebral venous thrombosis. JAss Phy Ind1998; 46: 706-07.

43. Fairburn B. Cerebral venous thrombosis complicating oral

contraceptice-anticoagulaent therapy. BMJ1973; 2: 647-8.

44. Kyritsia A, William EC, Schutta H. Cerebral venous thrombosis

due to heparin-induced thromocytopenia. Stroke1990; 21:1503-10.

45. Derex L, Philppean F, Nighoghossian N et al. Postpartumcerebral venous thrombosis. J Neurol Neurosurgery1988;

65 (5): 80-2.