The research paper published by IJSER journal is about Fatal tuberculous meningovasculitis 1

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Fatal tuberculous meningovasculitis

Oumerzouk J, Hssaini Y, Ait Berri M, Ragabbi A, El jouehari A, A Bourazza

AbstractTuberculous meningitis usually results in ischemic stroke, and rarely in hemorrhagic infarcts. We report a medicat history of a patient presenting a fatal outcome of tuberculous meningovasculitis. Brain MRI showed corticosub- cortical T2-Flair and Diffusion weighted hyperintense lesions within frontal lobe, temporal lobe and right cerebella hemi- sphere, with contrast enhancement.

Key words: Vasculitis, Meningoencephalitis, Mycobacteria tuberculosis, MRI, PCR

INTRODUCTION

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Tuberculous meningitis (TBM) usually results in ischemic stroke by arteritis. The clinical picture of strokes in TBM is polymorphous. Diffusion weighted imaging (DWI) provides information regarding tissue is- chemia at an early stage allowing rapid treatment. We report in this paper, a case report of a patient present- ing a fatal tuberculous meningovasculitis.

Case report:

A 45-year-old woman, previously healthy, ad- mitted to the hospital with a 15 days history of worsen- ing pancranial headache, confusion and fever with peaks at 40˚ C. She also complained of photophobia, nausea and recurrent vomiting. The neurologic symp- toms progress after 8 days to increasing weakness of the lower limbs. On neurological examination, the pa- tient was somnolent and disorientated, with bilateral sixth cranial nerve palsy and neck stiffness. Kernig's sign was positive. The patient was noted to have flaccid paraparesis (motor grade 4/5) with T8 sensory level. The deep tendon reflexes were present on the upper limbs and absent on the lower limbs. The plantar re- sponses were extensor. The cerebrospinal fluid was noted to be clear colorless and contained 10
RBCs/mm3, 560 WBCs/mm3 (96% lymphocytes), glu- cose 78 mg/dL (serum level, 229 mg/dL), protein 230 mg/dL. Contrast brain and spine MRI was unremarka- ble, but electroencephalogram showed diffuse slowing. Laboratory tests revealed hyponatremia of 125 mmol/l(normal 136-144) and CRP of 25 mg/l (nor- mal <7). Chest computed tomography scans showed bi-
lateral basal alveolar syndrome with airbronchogram
(figure 1) and real Time Mycobacteria tuberculosis PCR analysis performed on CSF was strongly positive. The patient was treated with 4 major antituberculosis and corticosteroids. Two days later, the patient presented sudden alteration of consciousness status immersing the patient in coma (GCS = 7). The patient was admit- ted in intensive care unit, where, performed brain MRI showed corticosubcortical T2-Flair and Diffusion weighted hyperintense lesions within frontal lobe (figure
2), temporal lobe (figure 3) and right cerebella hemi- sphere (figure 4), with contrast enhancement. The

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whole was suggestive of disseminated cerebral vascu- litis complicating tuberculosis infection. Unfortunately, despite a heavy treatment, the patient went into deep coma and passed away by cardiac arrest, 5 days after her intensive care unit admission.
Ischemic involvement of small and medium sized vessels at the base of the brain is a common complication in tuberculous meningitis (TBM).1TBM usually results in ischemic stroke but rarely it may result in hemorrhagic infarcts that are attributed to both arteri- al and venous thrombosis.2 Stroke in TBM occurs in 15
57% of patients. Many factors simultaneously play a role in its occurrence: stage of meningitis, hypertension, hydrocephalus, and exudates.3Most infarcts in TBM are as a result of hemodynamic hypoperfusion due to a var- iable combination of vasospasm, intimal proliferation and thrombosis of cerebral blood vessel walls 1. It is re- garded as a poor prognostic predictor of TBM.2
The pathophysiological mechanisms implicated in cere- bral vasculitis are diverse and can include: a direct pathogenic effect of the infectious agent on the vessels, role of cytokines (tumor necrosis factor, vascular endo- thelial growth factor and matrix metaloproteineases) in damaging the blood brain barrier, immunological in- volvement via the induction of antigen expression on endothelial cells and the formation of immune complex- es.1 In late stage, organization of basal exudates may strangulate the vessels leading to vascular narrowing and focal weakness.3The common pathological chang- es in cranial blood vessels in tuberculous meningitis are arteritis: Infiltrative, proliferative, necrotizing or fibrinoid necrosis. Vascular involvement starts in adventitia and progressively encroaches to involve the entire vessel wall constituting panarteritis tuberculosa.3 The uncom- mon complications include aneurismal dilatation, mycot- ic aneurysm, thrombus formation and venous sinus thrombosis.2 these different pathological changes prob- ably depend on the type, virulence of Myobacte- rium tuberculosis and on the host immune response to the infection.2
Most of the strokes in TBM are small, multiple, bilateral

and located in the basal ganglia especially the ‘tubercu-

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The research paper published by IJSER journal is about Fatal tuberculous meningovasculitis 2

ISSN 2229-5518

lar zone’ which comprises of the caudate, anterior thal- amus, anterior limb and genu of the internal capsule, corresponding to the deep sylvian region.1These are at- tributed to the involvement of medial striate, thala- motuberal and thalamostriate arteries which are em- bedded in exudates and likely to be stretched by a co- existent hydrocephalus. Cortical stroke can also occur due to the involvement of proximal portion of the mid- dle, anterior and posterior cerebral arteries as well as the supraclinoid portion of the internal carotid and basi- lar arteries.2 Small vessel occlusion is common in the early stage of TBM resulting in monoplegia whereas middle cerebral or internal carotid arterial territory in- farcts are common in advance stage resulting in hemi or quadriplegia.2 Vertebrobasilar territory strokes earlier have been reported to be rare but recently 20% of strokes in TBM have been reported in vertebrobasilar territory based on MRI study.2Arteries traversing the sulci of the vertex are usually unaffected.3
TBM related stroke most commonly manifests with in- sidious focal neurological deficit, acute confusional state, meningeal syndrome, headaches, cranial nerve paralysis, coma and seizures. The other neurological manifestations depend on the location of infarctions. A large stroke may result in raised intracranial pressure.2
Tuberculous cerebral vasculitis should be included in the differential diagnosis of any neurological deteriora- tion arising during the course of tuberculous meningi- tis.1
Diffusion weighted imaging (DWI) provides information regarding tissue ischemia at an early stage (within the first hour after stroke) as compared to conventional magnetic resonance imaging (MRI).4 DWI provided in- formation not available on conventional T2 weighted imaging in terms of the multiplicity of lesions and detec- tion of clinically unrelated area in a significant number of patients.4
MRA classically visualizes segmental narrowing, parie- tal irregularities and, sometimes, obstructions. Lep- tomeningeal vessels over the convexities of the brain may be stretched as a result of internal hydrocephalus or brain swelling. Sometimes luxury perfusion with early draining veins may be seen. Although the cerebral vas- culature can be visualized by MRA, direct angiography remains the gold standard for imaging the vascular lu- men.1
Corticosteroids should be prescribed in combination with antituberculous drugs to treat tuberculous meningi- tis.1This regimen were thought to reduce mortality and morbidity but their role in reducing strokes has not been proven. Aspirin also reduces mortality and its role in re- ducing stroke in TBM needs further studies.2

Conflict of interest The authors to have no conflict on interest

The authors want to thank BAYER S.A for partial fund support.

References:

[1].N.Javaud, S .Certal Rda , J. Stirnemann , AS.Morin , JM.Chamouard , A. Augier , O.Bouchaud , A/Carpentier
, R .Dhote , JL.Dumas , Fantin B, Fain O.Tuberculous cerebral vasculitis: retrospective study of 10 cases. Eur J Intern Med. 2011; 22(6):e99-104.
[2].UK. Misra , J.Kalita , PK.Maurya . Stroke in tubercu- lous meningitis. J Neurol Sci. 201115;303(1-2):22-30.
[3]. J.Kalita J, UK .Misra , PP.Nair . Predictors of stroke and its significance in the outcome of tuberculous men- ingitis. J Stroke Cerebrovasc Dis. 2009;18(4):251-8.
[4]. R.Shukla , A.Abbas , P.Kumar , RK.Gupta , S. Jha, KN.Prasad .Evaluation of cerebral
infarction in tuberculous
meningitis by diffusion weighted imaging.J Infect. 2008;57(4):298-306.

Acknowledgment

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Figure 3: Brain MRI showing Diffusion-weighted hyper- intense lesions in both temporal lobes.

Figure 1: Chest computed tomography scans showing bilateral basal alveolar syndrome.

Figure 4: Brain MRI showing Diffusion-weighted hyper- intense lesions interesting the right cerebellar hemi- sphere

Figure 2: Brain MRI showing Diffusion-weighted hyper- intense lesions at the internal part of frontal lobe.

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The research paper published by IJSER journal is about Fatal tuberculous meningovasculitis 4

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Author details

Oumerzouk Jawad, El Jouehari Abdelhafid, Hssaini, Yahya, Bourazza Ahmed

Authors affiliation:

Neurology department. Military hospital of Rabat. Mo- rocco

Corresponding author : Oumerzouk Jawad

Street address: Military hospital. Hay Ryad. Rabat. Mo- rocco
Number and postal code: 10100
Phone number: 00(212)670438897
E-mail: tamamro@yahoo.fr

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