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 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 24  |  Issue : 3  |  Page : 150-152

An unusual presentation of central nervous system tuberculosis with cerebral venous sinus thrombosis in a young male


1 Department of Internal Medicine, AFMC, Pune, Maharashtra, India
2 Department of Medicine, Command Hospital (SC), Pune, India
3 Department of Radiology, Army Hospital (R&R), New Delhi, India
4 Department of Surgery, Command Hospital (NC), Udhampur, India

Date of Submission31-Oct-2020
Date of Acceptance26-Dec-2020
Date of Web Publication01-Apr-2022

Correspondence Address:
Col (Dr) Rajagopal Srinath
Department of Internal Medicine, AFMC, Pune - 411 040, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jmms.jmms_161_20

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  Abstract 


Tubercular meningitis is prevalent in India as various clinical subtypes. Our case illustrates an unusual presentation of tuberculosis (TB) meningitis with cerebral venous sinus thrombosis. Our patient had presented with fever and headache for about 1 week, followed by acute onset left hemiparesis. His evaluation revealed features of cerebral venous sinus thrombosis (CVT) on neuroimaging along with cerebrospinal fluid picture of the central nervous system (CNS) TB. He was managed with antitubercular therapy with steroids and anticoagulation following which the patient recovered. The coexistence of CVT with CNS TB is very rare. It is pertinent to diagnose the same early to prevent life-threatening complications.

Keywords: Antitubercular drugs, central nervous system tuberculosis, cerebral venous sinus thrombosis, hemiparesis


How to cite this article:
Srinath R, Nanda SK, Mathur A, Sharma M. An unusual presentation of central nervous system tuberculosis with cerebral venous sinus thrombosis in a young male. J Mar Med Soc 2022;24, Suppl S1:150-2

How to cite this URL:
Srinath R, Nanda SK, Mathur A, Sharma M. An unusual presentation of central nervous system tuberculosis with cerebral venous sinus thrombosis in a young male. J Mar Med Soc [serial online] 2022 [cited 2022 Aug 14];24, Suppl S1:150-2. Available from: https://www.marinemedicalsociety.in/text.asp?2022/24/3/150/342377




  Introduction Top


The clinical manifestations of central nervous system tuberculosis (CNS TB), especially tubercular meningitis are highly variable depending on the age and comorbidities of the patient.[1] The cerebral venous sinus thrombosis (CVT) has been reported as a part of manifestations with some infectious conditions, especially Pneumococcal bacteremia. The presentation of CNS TB as a case of CVT is extremely rare with only few cases reported worldwide as yet. The treatment of these two coexisting conditions is much more challenging due to many factors.


  Case Report Top


A 37-year-old male, a shop keeper by profession with no previous morbidities, had presented with insidious onset low-grade fever, especially in the evenings along with moderate-intensity holocranial headache for 1 week, followed by acute-onset left-sided weakness of the upper and lower limbs in the month of February in 2016 to a tertiary hospital at Kolkata, India. On general examination, there were no peripheral markers of TB. Neurological evaluation revealed he was drowsy with a Glasgow Coma Score of E3V4M5 = 12/15. He had features of left hemiparesis with left upper motor neuron facial paresis with an extensor plantar response on the left side. He had meningeal signs in the form of positive Kernig's sign. There was no papilledema. The rest of his clinical examination did not reveal any abnormalities.

Investigations

The investigations revealed hemoglobin of 16.8 g/dl with normal erythropoietin levels and negative JAK-2 mutation. His total and differential white blood cell counts were within the normal range. The biochemical parameters including liver function test, renal parameters, and electrolytes were normal. The viral markers in the form of HIV/HBsAg/HCV were negative. A neuroimaging in the form of contrast-enhanced magnetic resonance imaging (MRI) of the brain and MR venography [Figure 1] revealed evidence of thrombosis of the sigmoid sinus and internal jugular vein on the left side. A cerebrospinal fluid (CSF) study revealed protein of 125 mg/dl and glucose of 27 mg/dl for a blood sugar of 156 mg/dl. The cell count was 250 with the predominance of lymphocytes. The CSF TB-polymerase chain reaction was positive along with elevated adenosine deaminase levels. The chest and abdomen computed tomography scan did not show any evidence of tuberculosis.
Figure 1: Magnetic resonance imaging and magnetic resonance venography of the brain showing thrombosis of the sigmoid sinus and internal jugular vein on the left side

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Treatment

He was started on antitubercular drugs in the form of isoniazid (5 mg/kg), rifampicin (10 mg/kg), pyrazinamide (25 mg/kg), and streptomycin (15 mg/kg intramuscular) along with steroid dexamethasone (0.4 mg/kg dose) tapered over 4 weeks in the Thwaite's protocol. He also received therapeutic anticoagulation with oral anticoagulants warfarin 5 mg/day after an overlap with low-molecular-weight heparin (enoxaparin 1 mg/kg/day BD) for a target international normalized ratio of 2.0.

Course in the hospital

By the beginning of the 2nd week, he had developed fresh obtundation of his sensorium which revealed evidence of hydrocephalus on repeat MRI for which an external ventricular drain was placed which was removed subsequently. The patient had a stormy course over the next few days which needed endotracheal intubation and ventilation for about 2 weeks, followed by T-piece oxygen requirement which was weaned off by 3rd week. He had developed fresh left hemiplegia in the 3rd week which revealed evidence of infarcts on MRI of the brain [Figure 2] in the right lentiform nucleus possibly due to tubercular arteritis which recovered gradually. Furthermore, he had developed hyponatremia with evidence of syndrome of inappropriate antidiuretic hormone secretion which was managed successfully. Over a period of the next 5 weeks, he recovered and became ambulant without support. The antitubercular drugs were continued for 18 months and anticoagulation stopped after 6 months and a procoagulant workup for Protein C, S, antithrombin III, and Factor V Leiden mutations and antiphospholipid antibody were also negative. His homocysteine levels were within the normal range. A repeat MR venography after 6 months showed recanalization of these sinuses.
Figure 2: Magnetic resonance imaging of the brain showing altered intensities in the right lentiform nucleus and corona radiata

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  Discussion and Conclusion Top


Tuberculosis affects more than one-third of the population across the world and more so in the developing countries.[1] In spite of a high prevalence of tuberculosis in India, the association of CNS TB with CVT is very rare. The exact pathophysiological mechanism of CNS TB causing CVT is unknown as yet. The possible postulated mechanisms might be (a) inflammatory endothelial injury, (b) venous stasis, (c) platelet aggregation, and release of pro-inflammatory mediators such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, CCL2, CCL5, and CXCL10.[2] The microglia infected by mycobacterium tuberculosis is found to produce robust immune response with TNF-α and IL-1β having additive effects on the endothelium.[3] The presentation of arteritis due to TB has been reported in the literature with possible mechanism of paradoxical thrombosis as the plausible explanation. It is not possible to conclude whether the association of CVT and tuberculosis is cause or effect.[4] A study evaluated 26 patients of TBM with the evaluation of cerebral arterial and venous system and the magnetic resonance venography (MRV) did not reveal any evidence of CVT, although variation in normal anatomy was seen in 14 (53.8%) patients, commonest being hypoplastic transverse sinus.[5] As yet, there are no guidelines or any available randomized control trials for the management of CVT due to infective origin. The duration of anticoagulation is also not clear in such cases and a minimum of 3 months anticoagulation is mandatory after which a workup for procoagulants if positive, the same can continue longer.[6] In our patient, a similar treatment protocol was followed and resolution of thrombosis was demonstrated in follow-up MRV, which was performed after a period of 6 months.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Rock RB, Olin M, Baker CA, Molitor TW, Peterson PK. Central nervous system tuberculosis: Pathogenesis and clinical aspects. Clin Microbiol Rev 2008;21:243-61.  Back to cited text no. 1
    
2.
Morioka H, Matsumoto S, Kojima E, Takada K, Iwata S, Okachi S. Paradoxical infarct in tuberculous meningitis: A case report. Intern Med 2012;51:949-51.  Back to cited text no. 2
    
3.
Pai N, Ghosh K, Shetty S. Hereditary thrombophilia in cerebral venous thrombosis: A study from India. Blood Coagul Fibrinol 2013;24:540-3.  Back to cited text no. 3
    
4.
Fiorot Júnior JA, Felício AC, Fukujima MM, Rodrigues CA, Morelli VM, Lourenço DM, et al. Tuberculosis: An uncommon cause of cerebral venous thrombosis? Arq Neuropsiquiatr 2005;63:852-4.  Back to cited text no. 4
    
5.
Kalita J, Singh RK, Misra UK, Kumar S. Evaluation of cerebral arterial and venous system in tuberculous meningitis. J Neuroradiol 2018;45:130-5.  Back to cited text no. 5
    
6.
Tufano A, Guida A, Coppola A, Nardo A, Di Capua M, Quintavalle G, et al. Risk factors and recurrent thrombotic episodes in patients with cerebral venous thrombosis. Blood Transfus 2014;12 Suppl 1:s337-42.  Back to cited text no. 6
    


    Figures

  [Figure 1], [Figure 2]



 

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