Cerebral venous sinus thrombosis is challenging condition because of its variability of underlying pathological causes. Numerous conditions can cause cerebral venous sinus thrombosis (CVST), and often more than one cause can be found in an individual patient. The causes leading to CVST can be classified into two broad categories; infective and non-infective. Among infective causes, chronic hepatitis C infection is considered as one of the extremely rare causes of cerebral venous sinus thrombosis

Anis, Anam

Athar, Iqra

Badshah, Mazhar

Khattak, Neelma Naz

Rajput, Haris Majid

English

eCommons@AKU

Pakistan Journal of Neurological Sciences (PJNS) Volume 15 Issue 3 Article 9 9-2020 Hepetatis c virus a rare cause of cereberal venous sinus thrombosis Haris Majid Rajput Pakistan Institute of Medical Sciences, Islamabad, Pakistan, Iqra Athar Pakistan Institute of Medical Sciences Islamabad Neelma Naz Khattak Pakistan Institute of Medical Sciences Islamabad Anam Anis Pakistan Institute of Medical Sciences Islamabad Mazhar Badshah Pakistan Institute of Medical Sciences Islamabad Follow this and additional works at: https://ecommons.aku.edu/pjns  Part of the Neurology Commons Recommended Citation Rajput, Haris Majid; Athar, Iqra; Khattak, Neelma Naz; Anis, Anam; and Badshah, Mazhar (2020) "Hepetatis c virus a rare cause of cereberal venous sinus thrombosis," Pakistan Journal of Neurological Sciences (PJNS): Vol. 15 : Iss. 3 , Article 9. Available at: https://ecommons.aku.edu/pjns/vol15/iss3/9 HEPETATIS C VIRUS A RARE CAUSE OF CEREBERAL VENOUSSINUS THROMBOSISP A K I S T A N  J O U R N A L  O F  N E U R O L O G I C A L  S C I E N C E S 3 8ABSTRACT:Cerebral venous sinus thrombosis is challenging condition because of its variability of underlying pathological causes. Numerous conditions can cause cerebral venous sinus thrombosis (CVST), and often more than one cause can be found in an individual patient. The causes leading to CVST can be classified into two broad categories; infective and non-infective. Among infective causes, chronic hepatitis C infection is considered as one of the extremely rare causes of cerebral venous sinus thrombosis.Keywords: Hepatitis C Virus, cerebral venous sinus thrombosisINTRODUCTIONCerebral venous sinus thrombosis is one of the rare condition which nowadays is being diagnosed more frequently due to greater awareness and availability of better diagnostic modalities. Predisposing factors can be identified in up to 80% of the patients. [2]   The main predisposing conditions causing cerebral venous sinus thrombosis are either infectious (causing 8% of cases in a series) or noninfectious. [2] Among non-infectious causes, the connective tissue disorders, granulomatous or inflammatory disorders and malignancies are the most frequent causes. [3] In addition 20% to 35% of the cases have no identifiable cause. [4] We report case of a 32-year-old male with chronic hepatitis C virus infection as an infrequent cause of cerebral venous sinus thrombosis. [5-7]CASE REPORTA 32 years old male patient presented with history of headache for less than 2 weeks, history of one episode of transient blurring of vision 1 week ago. Afterward he had an episode of generalized tonic-clonic seizure followed by development of left hemiparesis. There was no history of hypertension, diabetes mellitus, or drug intoxication. He is a known case of Hepatitis C virus for 3 months and is on anti-viral therapy Sofosbuvir and Velpatasvir for the past 3 months. On presentation his GCS was 8/15 (E3, M4, V1) with left sided weakness and a power of 3/5 in both upper and lower limbs. Cranial nerves and fundoscopy was normal. There were no signs of chronic liver disease on examination. His cardiovascular and respiratory examination was unremarkable. The initial laboratory tests including hematology, biochemistry and coagulation profile was normal. CT- brain was unremarkable. The initial laboratory tests including hematology, biochemistry and coagulation profile was normal. CT- brain was unremarkable. Magnetic resonance imaging (MRI) brain with Magnetic resonance venography (MRV) was done. MRI showed an infarct in right high parietal area (Figure. 1). MRV revealed superior sagittal sinus thrombosis (Figure 2). Antinuclear antibody (ANA) test was sent which came out negative.Figure 1. MRI brain plain. Coronal FLAIR (A) and T2 weighted Axial (B) images showing hyper intense signal in right high Parietal parafalcine region.Haris Majid Rajput1, Iqra Athar2, Neelma Naz Khattak3, Anam Anis4, Mazhar Badshah51.Consultant Neurologist, Pakistan Institute of Medical Sciences, Islamabad. 2,3,4 Postgraduate Resident Neurology, Pakistan Institute of Medical Sciences, Islamabad.5 Consultant Neurologist, Pakistan Institute of Medical Sciences, Islamabad.V O L .  1 5  ( 3 )   J U LY- S E P  2 0 2 0Correspondence to: Dr Haris Majid Rajput, Department of Neurology, Pakistan Institute of Medical Sciences, Islamabad, 44,000, Pakistan Email: : harismajid@gmail.comDate of submission: March 28, 2019  Date of revision: April 30, 2020 Date of acceptance: July 12, 2020C A S E  R E P O R TP A K I S T A N  J O U R N A L  O F  N E U R O L O G I C A L  S C I E N C E S 3 9Thrombophilia workup turned out to be negative including Lupus anticoagulant, Factor V Leiden, Anti thrombin-III, Protein C and S and PCR for thrombin Gene mutation (G20210A) (Table 1). His general and neurological examination after six months of treatment was unremarkable with full recovery of left sided body weakness.Table 1. THROMBOPHILIA SCREENING TESTSV O L .  1 5  ( 3 )   J U LY- S E P  2 0 2 0Figure 2. MRV brain.MRV shows signal void in middle part of superior saggital sinus.He was started treatment with anti-epileptics, anticoagulation and hydration. HCV PCR was repeated which was negative and antiviral drugs were stopped. Rivaroxaban was started in a dose of 15mg twice a day, which was later on switched to 20mg once a day after 3 weeks. With initiation of treatment dramatic improvement was seen, GCS improved to 15/15 and power of left side of body improved to 4/5 in both upper and lower limbs. After completion of six months of treatment with Rivaroxaban his neuroimaging was repeated. MRI brain with MRV scan which showed optimal visualization of superior sagittal sinus and no evidence of dural sinus thrombosis (Figure 3 and 4).Figure 3. MRI brain plain. T2 weighted Axial (A) and Coronal FLAIR (B) images showing resolution of lesion post therapy.Figure 4. MRV brain.MRV shows normal flow in all sinuses post therapy.DISCUSSIONCerebral venous sinus thrombosis results usually as a consequence of procoagulant conditions. [8] Cerebral venous sinus thrombosis has been described as a process of continued imbalance between prothrombotic and thrombolytic states, leading to progression of venous thrombosis with time. [2][ The mechanism by which cerebral venous sinus thrombosis occurs in patient with hepatitis B and C is not fully established, but it is thought that hepatitis is associated with formation of anti-cardiolipin antibodies. [9,10] Hence, the virus exclusively or in the combination with others such as anti-phospholipid syndrome results from formation of anti-cardiolipin antibodies during chronic hepatitis infection and can shift the delicate procoagulant/ thrombotic balance towards thrombosis.[7] However in our case anti-cardiolipin and other autoantibodies were negative. There are some data that suggest that HCV, itself might be responsible for thrombotic events.[6] It is hypothesized that protein that envelopes HCV has procoagulant activity and also virus genome that encodes for protein serine protease may have procoagulant activity. [11] In addition to that treatment used for HCV is capable of inducing variety of antibodies that also act as procoagulant. [12] Mostly this association is seen with INF-alpha drug. Since our patient was on sofosbusavir and velpatasvir, there is no documented data available for these two drugs that could possibly causing procoagulant state.CONCLUSIONIn conclusion, we suggest that Hepatitis C testing should be included in the investigation of unknown etiology of cerebral venous sinus thrombosis. Since our patient was known case of Hepatitis C and took oral antiviral therapy (sofosbusavir and velpatasvir) it is hypothesized that Hepatitis C virus uniquely is cause of cerebral venous sinus thrombosis.P A K I S T A N  J O U R N A L  O F  N E U R O L O G I C A L  S C I E N C E S 4 0 V O L .  1 5  ( 3 )   J U LY- S E P  2 0 2 0P A K I S T A N  J O U R N A L  O F  N E U R O L O G I C A L  S C I E N C E S 4 1Conflict of interest: There is no conflict of interest.. Funding disclosure: NilAuthor’s contribution:Haris Majid Rajput; data collection, data analysis, manuscript writing & reviewIqra Athar; manuscript writing, manuscript review Neelma Naz Khattak; data analysis, manuscript writing, manuscript reviewAnam Anis; data analysis, manuscript writing, manuscript review Mazhar Badshah; data analysis, manuscript writing, manuscript review V O L .  1 5  ( 3 )   J U LY- S E P  2 0 2 0References:1. Bousser MG, Russell RR (1997) Cerebral venous thrombosis. (W B Saunders, London).2.Villringer A, Mehraen S, Einhäupl KM (1994) Pathophysiological aspects of cerebral sinus venous thrombosis. J Neuroradiol 21:72–803. Ameri A, Bousser MG(1992) Cerebral venous thrombosis. Neurol Clin 10:87–111.4. Marques MCP, Pires LA, Damasceno CA, Felício AC, Atala A, Franco GM. Trombose da veia de Galeno: relato de caso. Arq Neuropsiquiatr 2003;61:285-2875. Pawlotsky JM, Yahia MB, Andre C, et al. Immunological disorders in C virus chronic active hepatitis: a prospective case-control study. Hepatology 1994;19:841-8486. Violi F, Ferro D, Basili. Hepatitis C virus, antiphospholipid antibodies, and thrombosis. Hepatology 1997;27:7827. Nadir A, Amin A, Chalisa N, van Thiel DH. Retinal vein thrombosis associated with chronic hepatitis C: a case series and review of the literature. J Viral Hepat 2000;7:466-470.  8. Beltrán-Blasco I. Trombosis venosas intracraneales. Rev Neurol 1997; 25:569-575.9. Prieto J, Yuste JR, Beloqui O, 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.         10. 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;72:690-692.   11. Bezan JF, Fletterick RJ. Detection of a trypsin like serine protease domain in flaviviruses and pestiviruses. Virology 1989;171:637-639.12. Saracco G, Touscoz A, Durazzo M. Auto antibodies and response to a-interferon in patients with chronic viral hepatitis. Hepatology 1990;11: 339-343  13. Sudhakar M Rao, Supriya Khardenavis, Aniurudda Deshpande, Suresh Pandi. Isolated vein of trolard thrombosis in an HBsAg- positive patient: case report. Medical Journal 2014;7:222-22414. André Carvalho Felício, Márcia Maiumi Fukujima, et al. Cereberal venous thrombosis and hepatitis: case report. Arq. Neuro 2006;7

Hepetatis c virus a rare cause of cereberal venous sinus thrombosis

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Hepetatis c virus a rare cause of cereberal venous sinus thrombosis

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