• cerebral venous thrombosis;
  • subarachnoid hemorrhage;
  • pseudotumoral cerebellar infarct


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  2. Abstract

Because of its large spectrum of clinical manifestations, diagnosis of cerebral venous thrombosis may be very difficult. Since appropriate treatment influences prognosis, early recognition of this condition is extremely important. We report a subarachnoid hemorrhage as a rare initial manifestation of cerebral venous thrombosis. A 58-year-old woman was admitted with severe headache of sudden onset, neck stiffness, dysarthria, and ataxia. Computed tomography scan showed a subarachnoid hemorrhage in the right posterior fossa. Magnetic resonance imaging coupled with magnetic resonance angiography revealed right transverse/sigmoid sinus thrombosis with hemorrhagic infarction of the right cerebellar hemisphere leading to a pseudotumoral appearance and displacing the fourth ventricle. Anticoagulant treatment resulted in rapid clinical recovery and in resolution of the radiological signs of infarction and of the subarachnoid and subdural hemorrhages.


cerebral venous thrombosis

Clinical expression of cerebral venous thrombosis (CVT) varies widely. Headache is the most frequent presenting symptom and may be associated in up to 50% of cases with papilledema.1 Focal cerebral signs, including motor or sensory deficits, dysphasia, and mental changes occur in approximately three quarters of all cases.1,2 Partial or generalized seizures may be encountered, particularly in isolated cortical vein thrombosis.3 Onset of symptoms is often acute if associated with occlusion of cerebral veins, and may be subacute or chronic if sinuses alone are affected. Here we report subarachnoid hemorrhage as a rare initial manifestation of CVT.


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  2. Abstract

A 58-year-old woman with a history of deep venous thrombosis after miscarriage at aged 30 presented with severe headache of sudden onset. The patient was on hormonal replacement therapy for the past 19 years, and her family history was positive for repeated deep vein thrombosis (mother and aunt). The headache was described as a thunderclap, involving predominantly the right temporal region. Concomitantly, the patient noticed blurred vision, gait imbalance, and dysarthria. One gram of acetylsalicylic acid and rest temporarily relieved the pain, which reappeared the next day, following physical effort.

On admission, she was afebrile, blood pressure was 130/50 mm Hg, and pulse was regular at 100 beats per minute; neurologic examination disclosed slight dysarthria and cerebellar signs of right upper and lower limbs. Gait was unstable. Cranial and cervical auscultation was normal. The neck was stiff. Consciousness, orientation, cranial nerve functions including ocular movements, and visual fields were normal. There was no papilledema. Laboratory tests revealed a normal sedimentation rate, normal whole blood count, and thrombocytes within normal range.

Head CT scan showed a right cerebellar subarachnoid hemorrhage and thrombosis of the right lateral sinus (Figure 1). Angiography disclosed thrombosis of the right transverse/sigmoid sinus but showed permeability of the superior sagital sinus and of the torcular; a dural arteriovenous fistula was not found. An MRI coupled with magnetic resonance angiography (MRA) performed 5 days later revealed right transverse/sigmoid sinus thrombosis and a right cerebellar hemorrhagic infarct with mass effect on the fourth ventricle (Figure). A low-molecular weight heparinoid at therapeutic doses was first administered and then replaced by an oral anticoagulant which has been continued (6 months follow-up). Dysarthria and ataxia disappeared completely, and the gait became normal after 4 weeks. A CT scan was then performed. It showed complete resolution of the hemorrhagic infarct and of the mass effect as well as disappearance of the subarachnoid hemorrhagic component. Coagulation studies including protein S, protein C, antithrombin III, and antiphospholipid antibodies were all negative, except factor II which showed a heterozygote prothrombin mutation (G20210A).


Figure 1.—. A shows brain CT scan after contrast injection showing thrombosis of the right sigmoid sinus (arrow); B, venous phase of magnetic resonance angiography (MRA) revealing thrombosis of the transverse/sigmoid sinuses (arrow); C, brain CT scan performed 10 days after admission demonstrating right cerebellar subarachnoid (arrow) and subdural hemorrhage and a venous infarct with mass effect and displacement of the fourth ventricle; and D, MRI performed 15 days after admission showing a cerebellar pseudotumoral venous infarct displacing the fourth ventricle (arrow).

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  2. Abstract

Subarachnoid and/or subdural hemorrhages have been very rarely reported in association with CVT. In their series of 110 patients, Bousser and colleagues described only 1 patient with headache of sudden onset as a presenting symptom of lateral sinus thrombosis.1,2 Some other rare case reports mention a similar clinical presentation. Ohta et al4 described a patient with aplastic anemia presenting a subarachnoid hemorrhage with thrombosis of the superior sagital sinus, and Zakharov and colleagues5 observed a spontaneous subarachnoid hemorrhage in a woman with an acute thrombus of the lateral sinus. Furthermore, a review of autopsy results of 353 patients who died of a subarachnoid hemorrhage did not demonstrate any case of CVT, suggesting that such an association is rather exceptional.6

Thrombosis of the transverse/sigmoid sinuses may extend into the cerebellar hemispheric veins thus causing their rupture. The superficial veins usually bridge the subarachnoid and subdural spaces near their site of entrance into the sinuses. They have thin walls, no smooth muscle fibers, and no valves, permitting dilatation and/or reversal of the direction of blood flow if the sinus into which they drain is occluded.1,7 This anatomical arrangement, as well as the important capacitance of the cerebral veins, may explain why clinical symptoms of subarachnoid and/or subdural hemorrhage occur so rarely, despite the fact that increased numbers of red blood cells may be found in the cerebrospinal fluid of patients with CVT.1,2

The first diagnosis suspected in our case was a posterior fossa dural arteriovenous fistula. These malformations, often associated with sinus thrombosis, may, in fact, present with clinical signs of subarachnoid and/or subdural hemorrhage.8 A few cases have been reported demonstrating the respective succession of these two vascular lesions.9 On the one hand, venous thrombosis may cause a fistula by opening of physiological shunts of the dura mater, diverting blood into the cortical veins and thus decreasing intracranial pressure. This phenomenon might consequently stop the spreading of the thrombus. Conversely, a dural fistula may induce occlusion of the adjacent sinus by alteration of venous return, stasis, compression, and progressive thrombosis. In a study comprising 77 patients, 1 of 51 patients with lateral sinus thrombosis developed a dural arteriovenous fistula; in 3 patients, a dural arteriovenous fistula was the underlying cause of the sinus thrombosis.10 A cranial bruit is often present in dural fistulas, but was absent in our patient. This differential diagnosis was further ruled out by angiography.

Cerebellar pseudotumoral infarcts of venous origin are very rare. To the best of our knowledge, only two cases have been reported.11,12 Although clinical signs of intracranial hypertension were not present in our case, CT scan and MRI clearly showed a mass effect with displacement of the fourth ventricle by the hemorrhagic infarct. Rousseaux et al reported one patient with venous thrombosis and pseudotumoral cerebellar infarction.11 In this case, clinical signs of intracranial hypertension were present and needed surgical intervention. Noteworthy, however, is the fact that the clinical course was progressive over 1 1/2 months until these clinical signs appeared. We, therefore, believe that in our patient, early anticoagulant treatment prevented a further progression towards intracranial hypertension. This treatment will be continued for life because of the factor II heterozygote prothrombin mutation (G20210A) and the increased risk of recurrence in patients with such an underlying thrombogenic condition.13

Our case demonstrates that CVT may simulate subarachnoidal hemorrhage from aneurysmal rupture and should therefore be considered in the diagnostic workup, since appropriate treatment of this condition influences prognosis.


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  2. Abstract
  • 1
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