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NI FEATURE: FACING ADVERSITY…TOMORROW IS ANOTHER DAY! - LETTER TO EDITOR
Year : 2017  |  Volume : 65  |  Issue : 3  |  Page : 626-628

Ruptured intracranial tuberculous aneurysm, a rare complication of central nervous system tuberculosis- A report and review of literature


1 Department of Medicine, Christian Medical College, Vellore, Tamil Nadu, India
2 Department of Radiology, Christian Medical College, Vellore, Tamil Nadu, India

Date of Web Publication9-May-2017

Correspondence Address:
Selvin Sundar Raj Mani
Department of Medicine, Christian Medical College, Vellore, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/neuroindia.NI_1280_16

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How to cite this article:
Mani SS, Mathansingh AJ, Kaur H, Iyyadurai R. Ruptured intracranial tuberculous aneurysm, a rare complication of central nervous system tuberculosis- A report and review of literature. Neurol India 2017;65:626-8

How to cite this URL:
Mani SS, Mathansingh AJ, Kaur H, Iyyadurai R. Ruptured intracranial tuberculous aneurysm, a rare complication of central nervous system tuberculosis- A report and review of literature. Neurol India [serial online] 2017 [cited 2019 Aug 23];65:626-8. Available from: http://www.neurologyindia.com/text.asp?2017/65/3/626/205897


Sir,

Tuberculosis is endemic and remains as a major health concern in developing countries like India. Central nervous system (CNS) tuberculosis is associated with an increased morbidity and mortality. The development of an intracranial tuberculous aneurysm is a rare complication of CNS tuberculosis. We report the case of a 45-year old gentleman with a ruptured intracranial tuberculous aneurysm. We emphasize its rarity and present a literature review of the previously reported cases.

A 45-year old gentleman presented to another hospital five months ago with a 2-month history of low grade intermittent fever, holocranial headache and non-projectile and non-bilious vomiting. He also had significant loss of weight and appetite. One month after the onset of fever, he developed weakness of the right upper and lower limbs associated with deviation of angle of the mouth to the left. Magnetic resonance imaging (MRI) of the brain done showed multiple ring enhancing lesions in the left fronto-parietal region with restricted diffusion in the centre, with the periphery of the lesions showing a well-defined T2 hypointense rim and oedema surrounding it [Figure 1]. He was diagnosed to be having a probable CNS tuberculosis with multiple tuberculomas and tuberculous meningitis based on the clinical picture, MRI findings and cerebrospinal fluid (CSF) analysis, at another hospital. He was started on a daily, weight-based regimen of anti-tuberculous treatment and steroids in tapering doses. His clinical condition had apparently improved with treatment. Four months after the onset of treatment, he presented to our hospital with a one-month history of low grade, intermittent fever followed by a one-day history of sudden-onset depressed sensorium, right-sided focal seizures and non-bilious, non-projectile vomiting. On examination, he was drowsy but arousable and was not oriented to time, place or person. His Glasgow coma score was E3V1M5 – 9/15. His vital signs were as follows: pulse rate of 90 per minute, blood pressure of 140/70 mm and respiratory rate of 20 per minute. He had paucity of movements, hypertonia of right upper and lower limbs with exaggerated reflexes and an extensor plantar response. Rest of the systemic examination was normal. His sensorium progressively worsened requiring endotracheal intubation. His MRI brain with contrast showed evidence of the previous abscesses in the left frontoparietal region, which had nearly completely resolved with anti-tuberculous therapy. An aneurysm was seen in the left middle cerebral artery branch in the Sylvian fissure with subarachnoid haemorrhage around the aneurysm. There was also evidence of leptomeningeal infiltration with the development of a new acute-to-subacute infarct in the deep perforator territory of the right middle cerebral artery. The cerebrospinal fluid (CSF) analysis showed a lymphocytic pleocytosis [total CSF count - 160 cells/cu.mm with predominant lymphocytes (68%)]. The CSF protein was 92 mg/dl and glucose was 134 mg/dl with a concomitant blood sugar of 160 mg/dl. He was considered to be having probable tuberculous meningitis according to the Lancet consensus diagnostic scoring system with a score of 13.[1] Subarachnoid haemorrhage due to the rupture of the left middle cerebral artery infectious aneurysm, secondary to the tuberculous CNS infection, was considered as the most probable diagnosis in view of clinical presentation and imaging findings. He was initiated on medical management of subarachnoid haemorrhage. He was continued on weight-based, daily, first line, anti-tuberculous medication and intravenous dexamethasone (0.4 mg/kg/day in 3 divided doses). Meanwhile, his condition progressively worsened and he succumbed to his illness.
Figure 1: (a) T1 post-gadolinium MRI scan showing a cluster of ring enhancing lesions; and, the centre on diffusion weighted image (DWI) being restricted (hyperintense), suggestive of an abscess –either pyogenic or tuberculous (Images taken at the onset of illness). (b) MRI T2 coronal and T1 post-gadolinium scans showing a flow void that intensely enhances, suggestive of an aneurysm. The aneurysm is arising from a branch of the left middle cerebral artery in the Sylvian fissure. DWI and apparent diffusion coefficient at the same time also shows new areas of abscess formation in the deep white matter along with the leptomeningeal disease in the right Sylvian fissure (short arrows on post-gadolinium scan)

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Tuberculosis (TB) still remains one the world's biggest threats. In 2014, there were around 1.5 million deaths worldwide, despite availability of effective anti-tuberculous drugs.[2] Tuberculosis of the central nervous system accounts for around 6% of extra-pulmonary tuberculosis.[3] It was first described as a distinct pathological entity in 1836. Complications of untreated tuberculous meningitis include obstructive hydrocephalus and obliterative vasculitis.[4] Obliterative vasculitis results in infarction and stroke syndromes, which account for several irreversible neurological sequelae.[5] However, a ruptured intracranial infectious aneurysm secondary to tuberculosis is a rare complication and is grossly under-reported. Only a few case reports of a ruptured intracranial tuberculous aneurysm have been published so far, the details of which are summarized in the [Table 1]. Kim et al., reported a case of subcortical mass (which was later diagnosed as a tuberculoma on biopsy) with adjacent multiple aneurysms involving the distal middle cerebral artery, that were noticed intraoperatively.[6] Intracranial tuberculous aneurysms can develop by two mechanisms:First, the hematogenous spread starts with septic embolization into the arterial wall via the vasa vasorum. This leads to degradation of the media and adventitia, proliferation of the intima and fragmentation of the internal elastic lamina. The bacteria seed into the intima of the vessel wall, which leads to arteritis and aneurysm formation. The other mechanism involves progressive weakening of the vessel wall due to encroachment of the adventitia by the thick inflammatory exudate. The pulsatile pressure of the blood in the weakened vessel leads to aneurysm formation.[3],[7] Diagnosis is established by magnetic resonance imaging of the brain and cerebral angiography.[8] Unruptured intracranial infectious aneurysms may be managed with antibiotics alone with a close follow up.[9] Ruptured aneurysms can be managed by surgical or endovascular treatment. Surgical management may be harmful and evacuation of the hematoma with a fragile aneurysm is associated with a high risk of rebeeding. It may be indicated in a young individual with a surgically accessible lesion or when associated with a large haematoma requiring evacuation due to the mass effect produced. Endovascular treatment involves embolization of the aneurysm using coils, cyanoacrylate or glue, which is applicable mainly for distally located aneurysms without significant ischemic brain damage.[10],[11] It is a safe mode of treatment with less incidence of immediate rebleeding and permanent neurological disability.[12] Prognosis of patients with a ruptured infectious intracranial aneurysm depends on its early recognition and aggressive management, and hence, a high index of suspicion is required.
Table 1: Summary of previously reported reports of ruptured intracranial tuberculous aneurysm

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Intracranial tuberculous aneurysm is a rare complication of CNS tuberculosis and a potential cause of death. Endovascular treatment is a safe mode of treatment for a ruptured aneurysm while invasive surgery is reserved for those patients having an associated large hematoma that requires evacuation due to its mass effect.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.[15]

 
 » References Top

1.
Marais S, Thwaites G, Schoeman JF, Török ME, Misra UK, Prasad K, et al. Tuberculous meningitis: A uniform case definition for use in clinical research. Lancet Infect Dis 2010;10:803-12.  Back to cited text no. 1
    
2.
Organisation mondiale de la santé. 006206416. Geneva: World Health Organization; 2015.  Back to cited text no. 2
    
3.
Saraf R, Limaye U. Ruptured intracranial tubercular infectious aneurysm secondary to a tuberculoma and its endovascular management. Br J Neurosurg 2013;27:243-5.  Back to cited text no. 3
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4.
Chatterjee D, Radotra BD, Vasishta RK, Sharma K. Vascular complications of tuberculous meningitis: An autopsy study. Neurol India 2015;63:926-32.  Back to cited text no. 4
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5.
Mahadevan A. The enigma of tuberculous vasculopathy-Is it time to review our dogmas? Neurol India 2016;64:864-7.  Back to cited text no. 5
[PUBMED]  [Full text]  
6.
Kim IY, Jung S, Jung TY, Kang SS, Moon KS, Joo SP. Intracranial tuberculoma with adjacent inflammatory aneurysms. J Clin Neurosci 2008;15:1174-6.  Back to cited text no. 6
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7.
Leiguarda R, Berthier M, Starkstein S, Nogués M, Lylyk P. Ischemic infarction in 25 children with tuberculous meningitis. Stroke 1988;19:200-4.  Back to cited text no. 7
    
8.
Garg RK, Malhotra HS, Jain A. Neuroimaging in tuberculous meningitis. Neurol India 2016;64:219-27.  Back to cited text no. 8
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9.
Phuong LK, Link M, Wijdicks E. Management of intracranial infectious aneurysms: A series of 16 cases. Neurosurgery 2002;51:1145-52.  Back to cited text no. 9
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10.
Cloft HJ, Kallmes DF, Jensen ME, Lanzino G, Dion JE. Endovascular treatment of ruptured, peripheral cerebral aneurysms: Parent artery occlusion with short Guglielmi detachable coils. AJNR Am J Neuroradiol 1999;20:308-10.  Back to cited text no. 10
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11.
Scotti G, Li MH, Righi C, Simionato F, Rocca A. Endovascular treatment of bacterial intracranial aneurysms. Neuroradiology 1996;38:186-9.  Back to cited text no. 11
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12.
Dhomne S, Rao C, Shrivastava M, Sidhartha W, Limaye U. Endovascular management of ruptured cerebral mycotic aneurysms. Br J Neurosurg 2008;22:46-52.  Back to cited text no. 12
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Roh JH, Park MH, others. A case of intracranial aneurysm and subarachnoid hemorrhage with tuberculous meningitis. Neurol Asia 2011; 16:157-61.  Back to cited text no. 13
    
14.
Modi M, Mochan A, Modi G, Hale MJ. Haemorrhage in intracranial tuberculosis. SA J Radiol 2005;9:16-18.  Back to cited text no. 14
    
15.
Griffiths SJ, Sgouros S, James G, John P. Intraventricular haemorrhage due to ruptured posterior inferior cerebellar artery aneurysm in tuberculous meningitis. Childs Nerv Syst 2000;16:872-4.  Back to cited text no. 15
[PUBMED]    


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