Development Of Cerebral Venous Thrombosis Research Articles

ID 366 – Cerebral venous thrombosis (CVT) in a female patient with severe obstructive sleep apnea (OSAS): Case presentation

Objectives Obstructive sleep apnea syndrome is reported to be a risk factor for arterial ischemic stroke, however, relationship between OSAS and cerebral venous thrombosis (CVT) remains uncertain. Case presentation We present a case of a 38-year-old obese woman, who developed headache, seizures and hemiparesis. Patient was taking combined oral contraceptive pills (OCPs) for 2 weeks prior to this event. Her coagulation profile (including ANA, anti dsDNA, antithrombin III, protein C and S and factor V leiden) was unremarkable. Magnetic resonance imaging (MRI) brain and magnetic resonance venography (MRV) were done and showed CVT. Patient underwent an overnight polysomnogram (PSG) which revealed severe OSAS. Conclusion Inspite of being a risk factor for venous thrombosis, short term consumption of OCPs cannot be considered as the only risk factor for the development of CVT in this patient, especially in the absence of hereditary thrombophilic state. In this obese patient, severe OSAS may be considered as another relevant contributory factor, which, together with the short term OCPs consumption, predisposes the patient to a state of hypercoagulability. Thus, OSAS should be considered as one of the multiple factors causing CVT.

Thrombosis of the cerebral veins in gynecological practice

The review presents literature data on the risk factors of cerebral venous thrombosis (CVT), a rare life threatening disorder. Currently, the diagnosis of CVT is made more often due to the possibility of using neuroimaging methods of cerebral structures. Pregnancy, postpartum period, use of oral contraceptives are risk factors of CVT. A role of thrombophilia, in particular Factor V Leiden mutations and the prothrombin G20210A polymorphism, in the CVT pathogenesis is confirmed. The development of CVT is an example of the interaction between persistent risk factors increasing the likelihood of thrombotic complications and acquired risk factors. A focal neurological deficit during pregnancy, delivery and postpartum period is the best indicator of CVT diagnosis. Possibilities of the use of anticoagulants in treatment and prevention of CVT are analyzed.

Cerebral venous thrombosis in two patients with spontaneous intracranial hypotension.

Although few patients with spontaneous intracranial hypotension develop cerebral venous thrombosis, the association between these two entities seems too common to be simply a coincidental finding. We describe two cases of spontaneous intracranial hypotension associated with cerebral venous thrombosis. In one case, extensive cerebral venous thrombosis involved the superior sagittal sinus and multiple cortical cerebral veins. In the other case, only a right frontoparietal cortical vein was involved. Several mechanisms could contribute to the development of cerebral venous thrombosis in spontaneous intracranial hypotension. When spontaneous intracranial hypotension and cerebral venous thrombosis occur together, it raises difficult practical questions about the treatment of these two conditions. In most reported cases, spontaneous intracranial hypotension was treated conservatively and cerebral venous thrombosis was treated with anticoagulation. However, we advocate aggressive treatment of the underlying cerebrospinal fluid leak.

Cerebral venous thrombosis after lumbar puncture and intravenous high dose corticosteroids: A case report of a childhood multiple sclerosis

The association between cerebral venous thrombosis (CVT) and multiple sclerosis (MS) has already been reported in several adult patients with clinically definite MS, in a suspected relation to i.v. corticosteroids or previously performed lumbar puncture (LP). We are reporting a case, which is, to our knowledge, the first one concerning a child patient with a MS, who developed multiple CVT after LP and during high-dose i.v. corticosteroid. Our conclusions are that the sequence LP followed by high dose corticosteroids may be a contributory factor for the development of CVT when associated with other risk factors.

Cerebral Venous Thrombosis in Spontaneous Intracranial Hypotension

The occurrence of cerebral venous thrombosis has been reported among patients with spontaneous intracranial hypotension, but a causal relationship has not been clearly established. We reviewed our experience with spontaneous intracranial hypotension and cerebral venous thrombosis and we reviewed the relevant literature to evaluate the relationship between these 2 entities. We reviewed the medical records and imaging studies of a consecutive group of patients with spontaneous intracranial hypotension evaluated at a tertiary care center between 1/1/2001 and 12/31/2007. The main search strategy was a systemic review of journal articles in MEDLINE (1966 to January 2008). Among 141 patients with spontaneous intracranial hypotension, 3 (2.1%) were also diagnosed with cerebral venous thrombosis. Among these 3 patients and the 17 reported in the literature there were 11 men and 9 women with a mean age of 39.5 years. Radiographic or clinical evidence for spontaneous intracranial hypotension preceding cerebral venous thrombosis was found in most patients, while there was no evidence for cerebral venous thrombosis preceding spontaneous intracranial hypotension in any patient. Eight (40%) of the 20 patients were found to have a change in their headache pattern believed to be due to the development of cerebral venous thrombosis. Complications of cerebral venous thrombosis, eg, cerebral venous infarction, occurred in 8 patients (40%). Spontaneous intracranial hypotension is a risk factor for cerebral venous thrombosis, but cerebral venous thrombosis is found in only about 2% of patients with spontaneous intracranial hypotension. A change in headache pattern is not a reliable predictor of the development of cerebral venous thrombosis in patients with spontaneous intracranial hypotension.

Contribution of multiple thrombophilic and transient risk factors in the development of cerebral venous thrombosis

Introduction Cerebral venous thrombosis (CVT), deep vein thrombosis (DVT) and/or pulmonary embolism (PE) have been associated with thrombophilic defects. However, in contrast to DVT or PE, CVT is a rare disease. We performed a study to identify differences in thrombotic risk profile, predisposing to CVT rather than DVT or PE, particularly the contribution of oral contraception and 11 thrombophilic defects. Materials and methods A single center case-control study (63 CVT cases and 209 controls with DVT or PE) was performed. Results Of CVT patients, 11% had experienced prior DVT or PE, and none had recurrent CVT at 5 years follow-up. CVT was more frequently observed in females (79% versus 51%, P < 0.001). It was more often secondary (75% versus 50%, P < 0.001), mainly due to the difference in age between both groups. At presentation of CVT and DVT/PE, oral contraceptives were used by 78% and 74% of non-pregnant fertile women ( P = 0.8), respectively. Any thrombophilic defect was demonstrated in 88% of CVT and 75% of DVT/PE patients ( P = 0.22), sex and age matched. Individual and two or more defects were equally distributed among both groups. Conclusions We conclude that a majority of CVT and DVT or PE patients show single or multiple thrombophilic defects. At presentation, oral contraceptive intake was observed more frequently in CVT patients. However, no differences were observed in thrombotic risk profile between both groups of comparable age. Hence, additional unknown risk factors should be considered to explain the different sites of thrombosis in these patients.

Cerebral venous thrombosis and demyelinating diseases: report of a case in a clinically isolated syndrome suggestive of multiple sclerosis onset and review of the literature

Cerebral venous thrombosis (CVT) has been described in several cases of clinically definite multiple sclerosis (MS). In the majority of these, lumbar puncture followed by intravenous corticosteroid treatment was suspected as the cause. We report what is, to our knowledge, the first case of a patient with a multifocal clinically isolated syndrome suggestive of MS onset, who developed multiple CVT after lumbar puncture and during high-dose i.v. corticosteroid treatment We conclude that the sequence 'lumbar puncture followed by corticosteroid treatment' may be a contributory risk factor for the development of CVT when associated with other risk factors.

Traumatic Intracerebral Venous Thrombosis Associated With an Abnormal Golf Swing

To describe the occurrence of cerebral venous thrombosis in a 40-year-old man whose cerebral event was induced by a poor golf swing, to review the literature on possible mechanisms producing venous thrombosis, and to compare this case with the literature. Headache is the most frequent symptom in patients with cerebral venous thrombosis. However, patients presenting with a headache due to cerebral venous thrombosis are uncommon. The known risk factors for thrombosis include both acquired and genetic factors. When the interaction of these two groups occurs, the magnitude of this interaction is thought to produce a dynamic state that can favor thrombosis. Our case report illustrates that moderate levels of anticardiolipin antibodies together with the mild trauma of a golf swing can induce a cerebral venous thrombosis. This case also suggests that although headache is rarely due to cerebral venous thrombosis, it should be excluded by good medical acumen and testing. Minor trauma induced by a poor golf swing was chronologically related to the development of a progressive cerebral venous thrombosis. The patient had none of the risk factors associated with a predisposition to venous thrombosis: hypercoagulable state, concurrent infection, pregnancy/puerperium, collagen vascular disorder, malignancy, migraine, false-positive VDRL, previous deep vein thrombosis, renal disease, factor V Leiden, or a hematological disorder. There was no anatomical abnormality that would predispose the patient to a cerebral venous thrombosis. The only laboratory abnormality was a moderate anticardiolipin antibody level (25 GPL). The patient was placed on warfarin sodium therapy and is currently without clinical sequela from the venous thrombotic event. Under certain circumstances, minor trauma can induce cerebral venous thrombosis. A review of the literature indicates that cerebral venous thrombosis in the presence of anticardiolipin antibodies and in the absence of systemic lupus erythematosus is a rare event. Previously, only major traumatic events have been reported to be associated with cerebral venous thromboses. The chronological development of cerebral venous thrombosis after a faulty golf swing strongly indicates that given a background of moderate levels of anticardiolipin antibodies, even minor trauma can induce a venous thrombotic event.

Cerebral venous thrombosis and anticardiolipin antibodies.

The association of cerebral venous thrombosis (CVT) with a variety of pathological states is well established. However, there are only rare isolated reports of CVT associated with anticardiolipin antibodies (aCL). To clarify the clinical and neuradiological features as well as outcome of patients with CVT associated with aCL, we reviewed the records of all patients with CVT evaluated at our institution between 1989 and 1996 (retrospective and prospective) and systematically reviewed the pertinent literature. We identified 8 aCL+ and 7 aCL- patients with CVT. No patients with lupus anticoagulant (LA) were identified. The mean age was 23 +/- 11.01 (range, < 1 to 36) years in the aCL+ and 38 +/- 9.30 (range, 25 to 54) years in the aCL- patients (P = .016). Six of 8 aCL+ and 5 of 7 aCL- patients were women. The dural sinuses were involved in all aCL+ and in 6 of 7 aCL- patients, while deep venous system thrombosis occurred in 5 of 8 (63%) aCL+ and 1 of 7 (14%) aCL- patients. In the aCL+ patients CVT was associated with puerperium or oral contraceptive use (n = 6), and sickle cell trait (n = 1), and in the aCL- patients CVT was associated with systemic lupus erythromatosus (n = 1), myelodysplasti syndrome (n = 1), colonic cancer (n = 1), oral contraceptive use or puerperium (n = 3), and dehydration (n = 1). Seven aCL+ patients received either intrasinus urokinase or intravenous heparin sulfate, and 1 received aspirin. Four aCL+ patients developed new onset or worsening of preexisting migraine, 2 developed recurrent peripheral venous thrombosis, and 1 went on to have intracranial hypertension. Twenty additional patients with CVT associated with antiphospholipid antibodies (aPL) were found reported in the literature. The overall mean age was 36 +/- 11.6 (range, 21 to 62) years, and 14 (70%) were women. LA was present in 11 of 18 tested, aCL in 7 (35%), LA and aCL in 1, and the type of aPL was not reported in 3. The mean age for the aCL+ only group was 28 years and for the LA+ (with or without aCL+) was 34 years. Only 1 patient, whose aPL type was not specified, had thrombosis of the deep venous system in addition to involvement of the dural sinuses. Our series and review suggest that aCL may be an important factor contributing to development of CVT even in the presence of other potential etiologies or risk factors. Onset of aCL+ CVT occurs at a relative young age and with relatively more extensive superficial and deep cerebral venous system involvement than aCL- CVT.

Cerebral Venous Thrombosis and Activated Protein C Resistance

Activated protein C resistance (APC-R) due to factor V Leiden has recently been established as an important risk factor for cerebral venous thrombosis (CVT). The clinical significance of abnormal or borderline functional APC-R in the absence of factor V Leiden is uncertain. Our observations suggest that APC-R due to mechanisms other than factor V Leiden may also contribute to the development of CVT. We describe three women who had superior sagittal and lateral sinus thrombosis while taking oral contraceptives and had a number of additional risk factors for CVT. Each had APC-R for different reasons. Inherited thrombophilia, including APC-R, should be looked for in all patients with CVT. Functional APC-R is a highly prevalent coagulopathy, but the reasons for this abnormality are diverse; abnormal and borderline functional APC-R results should be supplemented by DNA analysis for the presence of factor V Leiden.