**7. Tables**

124 Venous Thrombosis – Principles and Practice

slow, especially in patients with rapidly progreding symptoms and involvement of most of the dural sinuses and deep venous system. This patient population should be referred for thrombolytic treatment, as the overall mortality of these patients reaches 10%. (8-11) Our current experiences also point towards the possibility of mechanical revascularization of the obstructed venous bed, using the techniques of rheolytic thrombectomy and mechanical

Thrombophilic states are commonly observed in 25-35% of patients with venous thrombosis. (14,15) Hormonal contraceptives are currently used by more than 100 million women. Shortly after their introduction in 1960s, an increased incidence of thrombotic vascular complications was observed (16-18), together with an interaction of hormonal contraceptives and haemocoagulation system. Increased activity of coagulation factors VII, VIII, X and fibrinogen is a common finding in most cases. (19) Martinelli et al. in their work define the risk of onset of cerebral venous thrombosis in users of hormonal contraceptives OR 6,1 95% CI (3,3 – 11,00). This potential risk may be further intensified by congenital haemostatic

Peroral contraceptives induce extensive changes in the fibrinolytic system. The levels of plasminogen and plazmin-alfa2-antiplazmin complex are elevated, also the activity of tissue activator of plasminogen (tPA) is increased, at the same time, the level of antigen inhibitor of the plasminogen-I activator (PAI-I) and the PAI-I activity are decreased, and many other changes occur. The fibrinolysis in the users of contraceptives is elevated, which is most probably caused by the response and compensation of the prothrombogenic state, caused by hormonal preparations. These changes are identical in preparations containing levonorgestrel, as well as third-generation gestagens. (21) Genetically conditioned thrombophilic states of the fibrinolytic system (PAI-I) increase the potential risk of the onset of thrombosis in HAK users.

Hormonal contraceptives with third-generation gestagens are connected with an increased risk of venous thromboses, in comparison with previous generations of contraceptives. This risk is also present in women without V Leiden factor mutation or a positive family history. (23)

Our experience points towards the possibility of CVT onset in young women using hormonal contraceptives. This condition needs to be taken into account in cases of intracranial difficulties. CVT is most commonly manifested with headaches, vertigo and visual disorders. That is why the diagnosis should be considered when a sudden onset of such manifestations occurs in otherwise healthy young woman. The CT or MRI examinations should be directed towards the possibility of affection of the venous intracranial system. MRI and MR-venography or 3DX-RA venography significantly decrease the diagnostic process in patients with disorders of the deep venous cerebral system and a rapid development of symptoms. Direct endovascular thrombolysis, with the possibility of mechanical revascularization may dramatically improve the clinical course of patients with thrombosis of cerebral veins in patients with insufficient effect of anticoagulation therapy, associated with rapidly progreding disorders of consciousness. Thrombolytic therapy also decreases the occurrence of secondary complications following thrombolyses of cerebral veins, such as chronic intracranial hypertension with visual disorders or onset of arteriovenous shunts. (24,25) Taking into account the incidence of these serious complications, we consider as essential, in compliance with recommendations of the Czech Society of

disturbance of the thrombus with balloon catheters. (12,13)

An increased activity and clustering of platelets was observed. (22)

disorders. (20)

**6. Conclusion** 



Table 1. Age of patients included into the study

Table 2. Subjective and objective manifestations on admission

Cerebral Venous Thrombosis in Patients Using Oral Contraceptives 127

Leiden - - - - - - - - MTHFR ++ ++ +- +- - ++ +- +- PAI-1 - - ++ - - ++ +- +- Factor VIII - - - + + + - -

cysteinemia + - - - - - - -

deficit + - + - - - - -

deficit + + - + - + - +

n deficit - - + - - - - -

[1] Berenstein A, Lasjaunias P., Ter Brugge K.G: Venous Occlusive Disease. Surgical

Adults. Second edition, Springer-Verlag Berlin Heidelberg, 135-152; 2004 [2] Ferro JM, Canhao P, Stam J, Bousser MG, for the ISCVT Investigators: Prognosis of

[3] Forbes P.N.K, Pipe JG, Heiserman JE: Evidence for cytotoxic edema in the pathogenesis of cerebral venous infarction. AJNR Am J Neuroradiology 22;450-455, March 2001 [4] Peeters E, Stadnik T, Bissay F, Schmedding E et Al.:Diffusion-weighted MR imaging of an acute venous stroke. AJNR Am J Neuroradiology 22;1949-1952,November 2001 [5] Ducreux D,Oppenheim C,Vandamme X et Al.:Diffusion-weighted imaging patterns of

[6] Liang L, Korogi Y, Sugahara T et Al: Evaluation of the Intracranial Dural sinuses with a

[7] Majoie CHB, van Straten M, Venema HW: Multisection CT Venography of the dural

[8] Rael JR, Orrison WW Jr., Baldwin N, Sell J: Direct thrombolysis of superior sagittal sinus

Neuroangiography vol. 2.1 Clinical and Endovascular Treatment Aspects in

cerebral vein and dural sinus thrombosis, results of the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT). Stroke 35; 664-670, March 2004

brain damage associated with cerebral venous thrombosis. AJNR Am J Neuro-

3D contrast-enhanced MP-RAGE sequence: prospective comparison with 2D-TOF MR venography and digital subtraction angiography. AJNR Am J Neuro-

sinuses and cerebral veins by using matched mask bone elimination. AJNR Am J

thrombosis with coexisting intracranial hemorrhage. AJNR Am J Neuro-radiology

**-**MTHFR- methylentetrahydrofolate reductase, PAI- plasminogen activator inhibitor

Factor V

Hyperhomo-

Protein C

Protein S

Antithrombi

**8. References** 

Legend:- negative, +- heterozygous, ++ homozygous

Table 6. Results of thrombophilic parameters

radiology 22;261-268, February 2001

radiology 22; 481-492, March 2001.

18;1238-1242, Aug 1997

Neuroradiology 25; 787-791, May 2004.

**1. 2. 3. 4. 5. 6. 7. 8.** 


Table 3. Parenchymatous lesions on CT/MRI


Table 4. Occlusion of sinuses / cortical veins on DSA 3D- XR venography


LMWH – Low Molecular Weight Heparin, Wa – warfarin, LKT - local continuous thrombolysis

Table 5. Therapy


Legend:- negative, +- heterozygous, ++ homozygous

**-**MTHFR- methylentetrahydrofolate reductase, PAI- plasminogen activator inhibitor

Table 6. Results of thrombophilic parameters

#### **8. References**

126 Venous Thrombosis – Principles and Practice

Venous infarction,

Petechial

Sinus sagitalis

Sinus transversus,

Contraceptiv

Treatment

Outcome Complete

Table 5. Therapy

LMWH + Wa

recovery

LMWH + Wa

Complete recovery

Table 3. Parenchymatous lesions on CT/MRI

CT/MR **1. 2. 3. 4. 5. 6. 7. 8. %** 

vasogenic inflation + + + + + 62,5

haemorrhage + + 25,0

superior + + + + + 62.5

sigmoideus + + + + + + 75,0

Deep vein system + + + + 50,0 Cortical veins + + + + + 62.5 V.jugularis interna + + + 37.5 Cerebellar veins + 12.5

1. 2. 3. 4. 5. 6. 7. 8.

es + + + + + + + +

LKT + LMWH + Wa

Complete recovery

Smoking - - - - - - - -

LMWH – Low Molecular Weight Heparin, Wa – warfarin, LKT - local continuous thrombolysis

LKT + LMWH

Patient died

LMWH + Wa

Complete recovery

LMWH + Wa

Complete recovery

LMWH + Wa

Complete recovery

Table 4. Occlusion of sinuses / cortical veins on DSA 3D- XR venography

LKT + LMWH + Wa

Complete recovery

**1. 2. 3. 4. 5. 6. 7. 8. %** 


**8** 

**Cerebral Venous Sinus** 

*1Department of Neurology,* 

*1,2Bulgaria* 

*3Republic of Ireland* 

**Thrombosis - Diagnostic Strategies** 

*3Department of General Practice, Division of Population Health Sciences,* 

In 1825, Ribes described a case of a 45-year old man who died after a 6-month history of epilepsy, seizures and delirium. The autopsy examination revealed thrombosis of the superior sagittal sinus, the left lateral sinus and a cortical vein in the parietal region. This was probably the first detailed description of extensive cerebral venous sinus thrombosis (CVST). Since then, the literature describing this disease has comprised of case reports, series and some newer prospective studies, including recent reviews and guidelines (statement) on the diagnosis and management of CVST (Siddiqui & Kamal, 2006; Stam, 2005;

The cerebral venous sinus thrombosis is a challenging condition and it is most common than previously thought. CVST accounts for 0.5% to 1.0% of all strokes and usually affects young individuals. Important advances have been made in the understanding of the pathophysiology of this vascular disorder. The diagnosis of CVST is still frequently overlooked or delayed as a result of the wide spectrum of clinical symptoms and the often sub-acute or lingering onset. Patients with CVST commonly present with headache, although some develop a focal neurological deficit, decreased level of consciousness, seizures, or intracranial hypertension without focal neurological signs. Uncommonly, an insidious onset may create a diagnostic challenge. The main problem of this disorder is that it is very often unrecognised at initial presentation. In particular, a prothrombotic factor or a direct cause is identified in approximately 66% of the CVST patients (a list of most

Cerebral venous thrombosis is more common in women than men, with a female to male ratio of 3:1 (cited in Ferro & Canhao, 2011). The imbalance may be due to the increased risk of CVST associated with pregnancy and puerperium and with oral contraceptives. The female predominance in CVST is found in young adults, but not in children or older adults.

**1. Introduction** 

Saposnik et al, 2011; Brown & Thore, 2011).

important causal and risk factors are listed in **Table 1**).

**and Prognostic Models: A Review** 

Penka A. Atanassova1, Radka I. Massaldjieva2, Nedka T. Chalakova1 and Borislav D. Dimitrov3

*2Clinic of Psychiatry, Medical University, Plovdiv,* 

*Royal College of Surgeons in Ireland, Dublin,* 

