|Year : 2014 | Volume
| Issue : 2 | Page : 222-224
Case report of isolated vein of trolard thrombosis in an HBsAg-positive patient
Sudhakar M Rao1, Supriya Khardenavis2, Anirudda Deshpande3, Suresh Pandi3
1 Department of Medicine, Kasturba Medical College, Manipal, Karnataka, India
2 Department of Ophthalmology, JJM Medical College, Davanagere, Karnataka, India
3 Department of Neurology, Kasturba Medical College, Manipal, Karnataka, India
|Date of Web Publication||4-Feb-2014|
Department of Neurology, Kasturba Medical College Hospital, Manipal - 576 102, Karnataka
Source of Support: None, Conflict of Interest: None
Among the many infective causes of cerebral venous thrombosis (CVT), viral hepatitis is been regarded as a rare associated condition. We report on a 46-years-old man presenting CVT associated with hepatitis B infection. Hepatitis C being a rare cause of CVT is well documented in the literature. There is also mention of association of hepatitis B being associated with CVT to the best of our knowledge. Both these conditions are hypothesized as thrombogenic agents in the available literature, and further research is required to confirm the same. We suggest that virus B serology should be performed in the cases of cerebral venous thrombosis with unknown etiology.
Keywords: CVT in HBsAg-positive patient, isolated vein of trolard thrombosis, isolated vein of trolard thrombosis in HBsAg
|How to cite this article:|
Rao SM, Khardenavis S, Deshpande A, Pandi S. Case report of isolated vein of trolard thrombosis in an HBsAg-positive patient. Med J DY Patil Univ 2014;7:222-4
|How to cite this URL:|
Rao SM, Khardenavis S, Deshpande A, Pandi S. Case report of isolated vein of trolard thrombosis in an HBsAg-positive patient. Med J DY Patil Univ [serial online] 2014 [cited 2020 Jul 5];7:222-4. Available from: http://www.mjdrdypu.org/text.asp?2014/7/2/222/126354
| Introduction|| |
Isolated vein of trolard thrombosis is a part of superficial venous system of the brain, often located in post central sulcus, connects superficial middle cerebral vein of sylvius to superior sagittal sinus. Thrombosis of this venous sinus is a rare entity.
Similarly, amongst the rare causes of CVT, there are a few reports of hepatitis C being an etiological agent, and there is a single case report, which postulated the association of hepatitis B. The possible mechanisms described in the literature mention that these viruses either by themselves or in association with other factors may lead to thrombogenicity. These mechanisms are, however, not completely understood.
Hence, the possibility of a pathogenic role of occult hepatitis B virus (HBV) infection cannot be fully discarded, and requires molecular tests for HBV DNA detection. Nonetheless, we could find only one report of cerebral venous thrombosis associated to hepatitis B (HBV). That was the case of a 43-year-old male who presented with seizures and had a previous history of HBV. He developed a left transversal sinus thrombosis associated to left temporal posterior hemorrhagic infarct. On investigation, anti-cardiolipin antibodies were negative, though there was an anti-thrombin III, and protein C deficiency seen in the patient described.
| Case Report|| |
A 46-year-old man presented with occipital headache, throbbing in nature, associated with nausea and vomiting. Three days after this episode, he developed sudden onset left upper limb weakness and focal seizure with secondary generalization. Next day, he developed another episode of focal seizure with generalization. He had no past medical history and was a non-smoker without any history of drug or alcohol abuse.
General physical examination was unremarkable. Neurological examination revealed left-sided hemiparesis. Routine blood and urine examination were unremarkable.
Chest radiograph was normal. CT brain revealed right parietal area hyperdense lesion. MR Brain showed thrombosis of right vein of Trolard with late sub-acute venous infarcts in the subcortical white matter of right high parietal lobe with bleed within.
Investigations regarding possible secondary etiologies were carried out. ANA, IgG, and IgM anti-cardiolipins and ANCA were negative. Results from blood serology were as follow: VDRL negative; anti-HCV negative (enzyme immunoassay); HBsAg positive, HBeAg negative. Electrocardiography was normal. Echocardiography revealed normal biventricular systolic function with normal ejection fraction. Ultrasonography revealed cholelithiasis with normal liver echotexture.
Anti-coagulation was started with heparin and warfarin (target INR 2-3) along with anti-epileptics. Subsequent days, as the target INR was reached, heparin was stopped.
HBV DNA analysis, HBeAg were planned, but could not be done in view of financial constraints of the patient.
| Discussion|| |
Cerebral venous thrombosis is usually a consequence of these procoagulant conditions. Isolated cortical venous thrombosis is a relatively rare entity; fewer than 20 cases have been reported in the imaging literature. 
In the above text, [Figure 1], [Figure 2], [Figure 3] highlight Axial view of Susceptibility Weighted MRI Brain scan of the patient: Axial view of Susceptibility Weighted MRI Brain scan of the patient showing bloom in the region of thrombosed Vein of Trolard. [Figure 4] and [Figure 5] shows MR Venography showing non visualisation of Lt Vein of Trolard.
|Figure 1: Axial view of T1W Imaging of MRI brain of the patient Axial view MRI Brain showing T1W hyperintensity in the Vein of Trolard suggestive of thrombosis.|
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|Figure 2: Sagittal view T1W MRI brain imaging of the patient Sagittal view T1W MRI brain imaging of the patient suggestive of thrombosis of Vein of Trolard|
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|Figure 3: Axial view of Susceptibility Weighted MRI Brain scan of the patient Axial view of Susceptibility Weighted MRI Brain scan of the patient showing bloom in the region of thrombosed Vein of Trolard.|
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|Figure 4: Sagittal view MR Venography showing non visualisation of Lt Vein of Trolard.|
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|Figure 5: MRV showing normal flow through Superior Sagittal Sinus with non visualisation of Vein of Trolard.|
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Hepatitis C and B are well known to cause chronic active hepatitis. Rarely, chronic active hepatitis can be part of anti-phospholipid syndrome and may cause cerebral venous thrombosis.  In a study by Prieto et al. where 100 patients of chronic HCV infection with one or the other prothrombotic state were sampled, anti-phospholipid antibody was found to be positive in 22% patients of them. 
Other mechanisms of cerebral venous thrombosis in patients with hepatitis B and C, are not fully understood; there seems to be a consensus that these viruses individually or in combination, with a series of other factors, may lead to thrombosis. 
In absence of any other identifiable etiology, we focus the importance of hepatitis B and C to be routinely investigated to rule out cortical venous thrombosis of unknown etiology.
| Conclusion|| |
Both isolated vein of trolard thrombosis in itself and also in patient with HBsAg-positive status are very rare. The hypothesis of HCV (and maybe HBV) as thrombogenic agent deserves further attention.
We also suggest that HCV and HBV tests should be routinely included in the investigation of cerebral venous thrombosis of unknown etiology.
| References|| |
|1.||Leach JL, Bulas RV, Ernst RJ, Cornelius RS. MR imaging of isolated cortical vein thrombosis: The hyperintense vein sign. J Neurovasc Dis 1996;1:1-7. |
|2.||Kesler A, Pomeranz IS, Huberman M, Novis B, Kott E. Cerebral venous thrombosis and chronic active hepatitis as a part of the antiphospholipid syndrome. Post Med J 1996;72:690-2. |
|3.||Prieto J, Yuste JR, Beloqui O, Civeira MP, Riezu JI, Aguirre B, et al. Anticardiolipin antibodies in chronic hepatitis C: Implication of hepatitis C vírus as the cause of the antiphospholipid syndrome. Hepatology 1996;23:199-204. |
|4.||Felício AC, Fukujima MM, Fiorot JA Jr, do Prado GF, de Carvalho Filho RJ, Rodrigues CA, et al. Cerebral venous thrombosis and hepatitis. Arq Neuropsiquiatr 2006;64:1041-2. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]